Well, shit. Just as I mentioned ERV's post on HIV denial today, I read over at Respectful Insolence that Christine Maggiore has died from pneumonia. Maggiore, you may recall, made national news by refusing to take AZT while pregnant (although she was HIV positive). Her daughter, Eliza Jane, died at the age of 3 in 2005 from AIDS-related pneumonia. It would appear that her mother succumbed to the same illness:
According to officials at the Los Angeles County coroner's office, she had been treated for pneumonia in the last six months. Because she had recently been under a doctor's care, no autopsy will be performed unless requested by the family, they said. Her husband, Robin Scovill, could not be reached for comment.
As Orac notes, this is a tragedy on many levels. Maggiore and Eliza Jane both could have been on medications that would have allowed them to live essentially normal lives; now, a father and a young son are left to go on after the preventable deaths of half of their family. Maggiore also has devoted the past decade to spreading the notion that HIV does not cause AIDS, encouraging HIV positive mothers like herself to breast feed and refuse antiretroviral medications. And while Maggiore may be gone, that legacy lingers. My heart goes out to her family.
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Walter Gilbert will always be a dissident because private messages are not nearly as important as public statements. Gilbert is our father. Duesberg is our father. Lo is our father. Nicolson uncovered the day lily mycoplasma black op. Margulis is our mother. Dr. Fiala, ooh I would love it if she examined me baby...........Kary Mullis is a god to be worshipped. Dr. Col wear will lead us through battles.....there are hundereds more highly credentialed dissidents out there...........we've got the evidence and the scientists, most of the scientists on your side have not read a single paper on HIV pro orthodox or dissident,and they are too chicken to debate, all they can do is spam a website.
Let us have a moment of silence and seance for our scientific fathers.
Please repeat after me. " Googla palla walla walla" Let us chant in awe of our masters. Repeat this several times. (just collapsed in complete laughter)
There has been a long and persistent unwillingness to think again on the part of those who, originally in good faith, brought the HIV theory into being. There has therefore been much denigration, but never any scientific refutation of Duesbergâs critique.
The reasons for this unwillingness are best understood from two very early responses to the critique.
On 28 April 1987, less than two months after publication of Duesbergâs first paper on the subject, a memo was sent from the office of the Secretary of Health and Human Services (HHS) headed MEDIA ALERT. Copies were addressed to the Secretary, Under Secretary, and Assistant Secretary of HHS, and to the âAssistant Secretary for Public Affairsâ, the âChief of Staffâ, the Surgeon General, and âThe White Houseâ. The memo noted that:
"This obviously has the potential to raise a lot of controversy (If this isnât the virus, how do we know the blood supply is safe? How do we know anything about transmission? How could you all be so stupid and why should we ever believe you again?) and we need to be prepared to respond".
On November 17, 1988, John Maddox, the then editor of the influential science journal Nature, who rejected numerous submissions from Duesberg on HIV and AIDS, wrote to him:
"I am glad you correctly infer from my letter that I am in many ways sympathetic to what you say. I did not ask you to revise the manuscript, however. The danger, as it seems to me, is that the dispute between you and what you call the HIV community will mislead and distress the public in the following way. You point to a number of ways in which the HIV hypothesis may be deficient. It would be a rash person who said that you are wrong, butâ¦if we were to publish your paper, we would find ourselves asking people to believe that what has been said so far about the cause of AIDS is a pack of lies".
Concern for the public health, for the reputations of science and politicians, and good old-fashioned embarrassment, are all very human and understandable. Twenty-some years on, these same factors are still at work. In fact, they probably weigh even more heavily today on HIVâs âdiscoverersâ and on those who take up the cause of fighting the virus that was said to constitute such a threat to humanity.
But they do not constitute refutation of a leading scientistâs critique. Nor of the careful work contributed by many other scientists who have questioned the HIV orthodoxy, but whose views have been similarly kept out of the mainstream of scientific debate.
Yours,
Neville Hodgkinson
This much more accurately describes the HIV denialist movement itself. Seriously, you're posting shit from the 1980s. Do you have anything from this millennium?
But they do not constitute refutation of a leading scientistâs critique.
Sure they do. Even a child can see that.
But keep posting. You're amusing.
Hi Tara,
the bad thing about your blog is the huge number of dimwits it attracts...
Been a reader for a long time,occasional commenter,but I am put off by the wooists,liars and reality rearrangers you seem to attract.
Get a life,fuckheads.
Neville, it is AIDS denialist wingnuts such as yourself who have shown the persistent inability to âthink againâ, to consider new evidence, to develop, modify and even abandon theories when the evidence is against them. Unlike mainstream scientists. You exemplify your terminally fossilized thinking by boring us all yet again with your really, really dumb analysis of responses from over two decades ago. Your interpretation was dim-witted and insightless enough when you first came up with it. What makes you think endlessly repeating it year after will suddenly make it seem profound and worthwhile?
When you say, âThere has therefore been much denigration, but never any scientific refutation of Duesbergâs critiqueâ you simply red light yourself as utterly dishonest and untrustworthy. There are numerous scientific refutations of Duesberg, such as the Cohen (1994) articles in Science and studies which explicitly test Duesbergâs Drug-AIDS hypothesis from Ascher et al in 1993 to Chao et al in 2008. The fact that you choose personally to not accept the conclusions of these is of no consequence to anyone. No one gives a stuff what you think. The fact you tell outright lies by claiming they do not exist speaks volumes about your credibility.
You insult just about every HIV and AIDS researcher and physician on the planet by claiming they are collectively too dull to have critically examined the evidential basis of HIV causing AIDS. Your âsofteningâ of this claim by saying this failing is âunderstandableâ is beneath contempt.
And when you talk about the âcareful work contributed by many other scientists who have questioned the HIV orthodoxyâ who the hell are you talking about? Do you mean the Mirth Group clowns who tried to convince the South Australian Supreme Court they were genuine HIV/AIDS experts despite having done no formal study or training in the relevant fields, never encountering a patient, and never completing even an hoursâ worth of productive research in the field? Or do you mean buffoon-extraordinaire Henry H. Bauer who wrote a book focusing on the epidemiology of an infectious disease while never bothering to familiarise himself with either the basics of epidemiology or the the basics of the disease he pretends to examine?
"Even if HIV signed a written confession, he'd claim it was coerced."
Don't give up cooler! Your strong showing has inspired all of us here. In fact, we've all taken it upon ourselves to inject isolated HIV into ourselves! Woohoo!
Now we just wait ten years and see if any of us get AIDS. I bet we won't. Don't you?
Say... do you want to join us? I'm sure you are confident enough to test your theory... right? You aren't in fact a lying pussy... right?
How about this? We can really show them if me and you get together with any two of these HIV-AIDS morons that actually has HIV.
They can put their money where their mouth is by getting regular AZT treatments, at the same time we can get regular HIV infusions. When they die, we win! Woot!
(No autopsies if we coincidentally die first though, you know they'd just twist the evidence to indicate it was somehow mysteriously AIDS, even though there's no way we could have caught it. (You don't take drugs right? Not even your psych meds?))
Of course he doesn't take those things. Cooler is smart enough to know that psychiatric drugs suppress the immune system, which leads to the so-called AIDS. Also, loneliness, stress, and paper cuts can cause "AIDS". Actually, pretty much anything can lead to AIDS, except for HIV. Just ask your friendly neighborhood nutcas^H^H^H^H^H^Hre-thinker.
It's really a shame how denialists are trying to deny the obvious: That Maggiore died of complications of longstanding untreated HIV.
ORAC,
Surely you're a ghoul! She died of radical detox and stress and television! These can all lead to disseminated herpes and multiple bouts of pneumonia. No, we don't need proof of this, anonymous people all over the AME boards have claimed this and that is evidence enough for us!!!
I see that many AIDS denialists use the word "Evidence" quite often.
They claim to "want" evidence.
They then will deny any evidence placed in front of them that doesn't fit with their pre-conceived conclusions.
They deny, deny, deny, deny... and the toll of deaths that would have been drastically delayed if not for their stupid, uninformed, evil woo-meistering keep climbing as they shriek their idiotic refrain:
"It wasn't AIDS! AIDS DOESN'T EXIST! IT CAN'T EXIST BECAUSE I DON'T WANT IT TO! These people died of bad humours in the blood, or stress, or a gypsy curse or something else... ANYTHING else!"
Sickening. So very sickening.
Hate to break it to you, you woo-addled twat-waffles: AIDS exists. It is caused by the HIV virus. It kills people. It can be treated to drastically increase life expectancy and lower the chances of transmission to loved ones during normal daily contact.
To deny the evidence in order to promote your favorite brand of snake-oil, or in some misguided or evil attempt to sweep it under the rug is to cause many others to die.
My friend, John Higgins, died of AIDS in 1991. He was diagnosed as HIV positive in 1990. The last year of his life was spent in the fight to make others aware that HIV and AIDS were treatable, preventable, and the concern of every single person living on the planet, be you male, female, gay, straight, conservative or liberal.
Deny it all you want, but HIV and AIDS are out there, they are real and no amount of whining or wishful thinking on your part is going to change that fact.
Every person that dies a day sooner than they should have from listening to you denialists and your bullcrap is a death for which you are responsible. Those deaths are on you. THOSE DEATHS ARE YOUR FAULT AND YOU ARE NO BETTER THAN MURDERERS.
How unpleasant to see Neville Hodgkinson appear in this thread. People like cooler I can tolerate, since he is merely delusional, and in all probability entirely harmless. But Hodgkinson, with his devious and spectacularly untruthful denialist books and media publications, has probably done more than Maggiore herself to lead people down the road to an early and untimely death. I hope his posting was just a drive-by, since I can sense my nausea rising and don't wish to read his tripe again.
Kate,
You yourself are "Sickening. So very sickening."
"Hate to break it to you, Kate, you woo-addled twat-waffle:" AIDS has NOT been proven to exist, kill t cells, or be sex xmitted. The HIV virus IS A MEME. Lots of things, and factors cause immune suppression and kill people. If it can be treated to drastically increase life expectancy and lower the chances of transmission to loved ones during normal daily contact, then PROVE IT WITH SCIENTIFIC STUDIES.
To deny the evidence in order to promote your favorite brand of snake-oil, or in some misguided or evil attempt to sweep it under the rug is to cause many others to die.
Your friend, John Higgins, died not of AIDS, but of high dosage AZT and stressing himself to sickness in 1991.
Deny it all you want, but HIV and AIDS are founded in BS, and they are unproven to be related and no amount of whining or wishful thinking on your part is going to change that fact.
Every person that dies a day sooner than they should have due to liver failure, suicide, or toxic aids drug effects from listening to you reality denialists and your bullcrap is a death for which you are responsible. Those deaths are on you. "THOSE DEATHS ARE YOUR FAULT AND YOU ARE NO BETTER THAN MURDERERS".
If you want to claim the dissidents are responsible, then whip out the studies and PROVE IT!
Hey PROVE IT is back. Here let me re-post this for you then in case you missed it:
âFurthermore, all the HIV experts including Gallo and Montagnier â¦were aware that this template-primer can be transcribed by cellular DNA polymerases, and this was also proven by Montagnier himself in 1984.â
How dense can you possibly be? This was already answered in my previous post if you bothered to read the quotation from the Montagnier paper that indicates why the RT activity detected was NOT an artifact of cellular DNA polymerase. Here let me repeat what the paper itself said. Maybe if you read it again a second (or first) time youâll understand it:
Virus-infected cells from the original biopsy as well as infected lymphocytes from the first and second viral passages were used to determine the optimal requirements for reverse transcriptase activity and the template specificity of the enzyme. The results were the same in all instances. The reverse transcriptase activity displayed a strong affinity for poly(adenylate - oligodeoxythymidylate) [poly(A) - oligo(dT)], and required Mg2+ with an optimal concentration (5 mM) slightly lower than that for HTLV (14) and an optimal pH of 7.8. The reaction was not inhibited by actinomycin D. This character, as well as the preferential specificity for riboseadenylate * deoxythymidylate over deoxyadenylate * deoxythymidylate, distinguish the viral enzyme from DNA-dependent polymerases.
OK, all clear now!? Do you understand how they knew this wasnât a cellular DNA polymerase or should I make sock puppets and act it out for you?
âIs there some part of the following that you are unable to read or understand? However, in 1984 Gallo and his colleagues said that Montagnier and his group's 1983 evidence did not prove "true isolation".
When did this become about isolation? The subject was about whether there was evidence that HIV was endogenous. I realize you are trying to change the subject but you are the one that brought it up when you claimed HIV could âfor all you knowâ be a hERV.
âThis CLEARLY INDICATES that the study you are attempting to use as proof is disqualifed until you present evidence that these very clear factors have been refuted.â
What seems âCLEARâ to you is obviously a product of your lack on understanding. We were using this paper in discussing whether proof existed of HIV being endogenous, not whether it was isolated at that time isolated.
So here are my questions to you:
1) Do you concede that there is ample evidence that HIV is not endogenous based on
*RT activity in infected but not control cells of cord blood.
*RT activity in infected but not control cells of adult cells.
*The RT activity demonstrated did not fit that of cellular DNA polymerase
* HIV is a lentivirus, of which there are NONE endogenous to humans.
2) Do you admit that you did not bother to read the Montagnier paper but rather relied on denialist BS for your arguments?
And to end it I would like to give us all a moment of pause to see why Cooler will never be convinced of his own stupidity:
"After all if eliza did die of AIDS shoulndt christine be dead by now since she was positive in 1992, what ad hoc excuse do you boneheads have for that?"
Hey Cooler...? EPIC FAIL!
"Prove it", you're an idiot. You know nothing of John's condition at the time of hid death, his symptoms or what treatments he was receiving at the time, and yet you claim to know what killed him.
I see no reason to engage someone so dishonest in further discussion.
my oh my, where do all those denial trolls come from?? Do they breed them, or is this an evolutionary step that will solve overpopulation??
all those trolls are potential Darwin Award winners and wouldn't it be for the innocent and unknowing along the way that get hurt by those ignoramuses one could jest let them go on removing themselves from the gene-pool.
"Prove it", you're an idiot. You know nothing of John's condition at the time of hid death, his symptoms or what treatments he was receiving at the time, and yet you claim to know what killed him.
I see no reason to engage someone so dishonest in further discussion."
Strange yet you all know everything about Christine's death, You guys don't know diddly, her tcell count to see if he even had "AIDS", her medical records to see if she was even HIV positive. Nothing. Dumbass losers.
"Strange yet you all know everything about Christine's death, You guys don't know diddly, her tcell count to see if he even had "AIDS", her medical records to see if she was even HIV positive. Nothing. Dumbass losers."
Strange, it didn't seem to matter to you when you paraded her being alive as proof you were right.
Poods, considering that you asked so nicely, you certainly deserve an answer to the foolowing questions you posted:
"So here are my questions to you:"
"1) Do you concede that there is ample evidence that HIV is not endogenous based on
*RT activity in infected but not control cells of cord blood.
*RT activity in infected but not control cells of adult cells.
*The RT activity demonstrated did not fit that of cellular DNA polymerase
* HIV is a lentivirus, of which there are NONE endogenous to humans.
The answer is rather simple, Poods. Please remember that at that time in 1984, RT was considered to be evidence of retroviral activity. As it is well demonstrated that RT is very common and quite often has nothing to do with any endogenous or exogenous retroviruses, the only evidence that would have been sufficient would have been to verify via EM patient actual patient sera to the lab cultures so that the proposed results were linked and verified.
They were not. So BIG NO. Insufficient evidence. And also not repeated or backed up by other labs with any fuller evidence such as linking the same RT in hiv positives to EM's.
You have a fluke that could have been anything at all, including RT due to fungal contaminations of the cultures, or who knows what all else.
2) Do you admit that you did not bother to read the Montagnier paper but rather relied on denialist BS for your arguments?
No, I do not admit to this because yes, I read the study. And. It is fully insufficient and is not backed up by replication or EM verifications to patient sera.
And either way, even if the results do somehow show an endogenous retrovirus, we are still missing the links to observed harm to any T-cells. We are still missing evidence of sexual transmission. We are still missing evidence of immune suppression causation.
So keep those studies coming, and lets see if you can somehow shut the denialists down with the presumed "evidence" that is claimed to be somewhere, all neatly linked together, in that great big "PIE IN THE SKY" (or should I say hole in the ground), commonly referred to as the "MOUNTAIN OF EVIDENCE" showing hiv is isolated from human sera, is the causative factor of any immune suppression, is sexually transmitted, and, that this mysterious boogeyman that has yet to have any found mechanism for doing so, is somehow the true cause of aids.
As I have said, repeatedly,
PROVE IT OR ADMIT YOU ARE WRONG!
DT,
in your statement: "But Hodgkinson, with his devious and spectacularly untruthful denialist books and media publications..),
you are presenting clear evidence that Hodgkinson is absolutely correct in his statement: "There has therefore been much denigration, but never any scientific refutation of Duesbergâs critique".
And that you yourself are also the very proof of his Neville's claim.
Kate, you woo-addled twat-waffle,
You said: "You know nothing of John's condition at the time of hid death, his symptoms or what treatments he was receiving at the time, and yet you claim to know what killed him".
The ONLY DRUG being given to ALL HIV positives in 1991 when John was diagnosed and died, WAS HIGH DOSAGE AZT MONOTHERAPY.
As you wish to decieptfully cover up the facts of John's death, I see no reason to engage someone so dishonest as yourself in further discussion.
ROFLMAO! You've been hoisted by your own petard Cooler! You used her as evidence that HIV+ people don't die in that comment, and now you're trying to use her as evidence that people who aren't HIV+ die of pneumonia anyway.
Have some damn consistency, or at least admit you were badly badly mistaken at least once!
No, I mostly rely on the peer review literature, like when Gallo and Levy could only isolate HIV in 26/72 patients and 22/45 patients respectively. Levy found almost the same amount of Antibodies to HIV in AIDS that he did in Non AIDS patients. Not that finding antibodies mean anything since everybody has antibodies to the flu, measles etc. Pretty sad that the whole HIV theory is based on partial poor correlations. No wonder you all are shit scared to debate Duesberg.
"Antibodies to ARV were found in all 86 AIDS patients and in a high percentage of 88 other homosexual men in San Francisco."
Levy, et al 1984 Science
CAN YOU ALL SHUT THE FUCK UP!
Me and PROVE IT and Cooler are all going to inject ourselves with HIV to SHOW you little morons that HIV doesn't cause AIDS.
All you need to do is provide 3 people who already have HIV who are willing to inject the POISON AZT!
We will all take our respective injections, and show you guys that SCIENCE DOESN'T MEAN SHIT!
I know someone who has HIV and HASN'T DIED! Her name is Christine and she... wait I mean I've NEVER heard of anyone who has DIED of HIV, the only person who has died recently DIDN'T have HIV and died OF NORMAL DEADLY PNEUMONIA. Idiots. Her daughter died of other non-hiv stuff too. Premature mother-daughter deaths often happen in people living near... trees, power stations etc. There's infinite causes, so shut up
âNo, I do not admit to this because yes, I read the study. And. It is fully insufficient and is not backed up by replication or EM verifications to patient sera.â
So you are saying that you read it and yet you:
a) did not realize that adult cells and not just cord blood was used, despite the fact that half the paper dealt with adult cells and
b) were not aware somehow how they knew the RT activity was not cell DNA polymerase.
Do you really expect us to believe this? Had you read the study you would have been aware of these factors (and many others). So did you:
A) Read it and simply lack the understanding
B) Read the paper but skip roughly half of it
C) Read the paper, understand it and outright lie
D) Not read it at all.
I am betting that D is the most probably case. If it wasnât, however, I would like to ask how you could believe yourself competent to comment on this paper (and others) with the reading skills or comprehension you will have displayed if option A or B were correct?
LISTEN POODLE you'd better PROVE IT OR ADMIT YOU'RE WRONG!!!
Wait, what's that you say? You have proved it? Well let me read your really really stupid posts...
...
...
...
...
Oh, well shit. You HAVE proved it, to a ridiculously effective degree. In fact, you've PROVED IT to such a degree that only those completely unwilling to read your posts could possibly have missed it.
I GUESS YOU'VE PROVED IT and EVERYONE DISAGREEING WITH YOU IS WRONG!
Silly me.
Hey, you three! Are you going to INJECT IT OR ADMIT YOU'RE WRONG?
Because if you don't INJECT IT OR ADMIT YOU'RE WRONG then we know you either don't really believe what you're saying, or you just don't have the balls to trust your own arguments!
IIOAYW!
IIOAYW!
IIOAYW!
Poods,
Are you claiming that that the reverse transcriptase activity found in this study is sufficient to determine that hiv was the cause of the RT?
Please explain how the study confirms that hiv could be the only cause of RT activity in a lab that fully admitted that contaminations of cultures were a frequent occurrence?
And Poods,
Could you please explain to us just how the indirect evidence of finding RT expressions, without EM's of the presumed retrovirus found in the sera of the supposedly infected individuals, is sufficient to determine a retrovirus?
And even if it did, just how are you backing up that the supposed retrovirus is the cause of any immune suppression?
Do you have any studies that back any of this up?
The reason I ask, is because many factors have been found that lead to RT expression.
And you have not presented any evidence of any supposed retrovirus in existence doing anything at all.
So far, Poods, all you have verified is the following;
1) Failure to prove the existence of a unique, exogenously acquired retrovirus, HIV.
2) Failure to verify the HIV antibody tests proof of HIV infection.
3) Failure to prove HIV causes immune deficiency (destruction of T4 lymphocytes) or AIDS.
4) The impossibility of haemophiliacs acquiring HIV following factor VIII infusions.
5) Failure to prove the HIV genome, (RNA or DNA) originates in a unique exogenously acquired infectious retroviral particle.
6) Failure to prove HIV/AIDS is infectious, either by blood, blood products or sexual intercourse.
7) Failure to prove what is called AIDS in Africa or Thailand is caused by HIV or is sexually transmitted.
8) Failure to disprove that AIDS and all the phenomena inferred as "HIV" are induced by changes in cellular redox brought about factors other than a retrovirus.
9) Failure to show that AIDS will not spread outside the original risk groups
10) Failure to disprove any of the pharmacological data that do clearly show AZT cannot kill HIV and failure to disprove that AZT is toxic to all cells and causes AIDS.
So, keep going Poods! You are doing great. You are on a real roll here, and have almost made a dent in Number One on this list!
Minor correction to # 9 above.
Should read:
Failure to show that AIDS WIll spread outside the original risk groups.
Prove It,
I would be happy to but if you don't read the paper yourself how can you understand it? So I ask again:
Did you:
A) Read it and simply lack the understanding
B) Read the paper but skip roughly half of it
C) Read the paper, understand it and outright lie
D) Not read it at all.
There is much more to the paper than you have read about in denialist websites. Think of this (and I say this not as an insult but rather as something to seriously consider):
Up to at least 2 days ago you were under the impression that
1) Montagnier did not use adult cells, only cord blood cells and
2) that the RT activity could be cell DNA polymerase activity but had no clue that Montagnier ran controls to test for this.
All this was clearly obtained from denialist postings (in fact I found some of your post word for word on other sites) but clearly the paper was not read.
So here is what you should seriously consider: If the sources of information you hold so dear have lied to you in these two instances (and these are from only one paper and on two pretty major points) what else could you be misunderstanding due to denialist sites that you take at face value with no further research?
Do you see why people are not exactly chomping at the bit to cite papers that, for example, demonstrate sexual transmission?
In addition to: "If the sources of information you hold so dear have lied to you in these two instances...what else could you be misunderstanding..."
I will add: If they (denialist information sources) will lie to you about such easily verifiable and very relevant facts, why should ANYONE take them as a credible authority?
Poodle, poodle, poodle!
You ask a good question: "why should ANYONE take them as a credible authority"
But take it a step further. Why should anyone take ANYONE as a credible authority and blindly follow them?
No need to work yourself into a frazzzzzle!
I do understand and know you mean well. I really really really do.
However, to me, you are still lost in the weeds, boy. I would very much like to see you rise above those weeds and I encourage you to see the bigger picture, though I cannot do that for you. I can only encourage you to step outside of your preconceived beliefs and need for "authorities" such as Tara, Orac, Gallo, or even Maggiore, Duesberg, and the Perth Group, and just do it for yourself.
If you don't like what you see from there, or if it is too scary for you at such altitudes of higher life views, then you can always fall back down and go back into the weeds after!
And as I said, I really do know that you mean well. So do Snout, DT, Orac, Srsly, Kate, Tara, etc, etc, etc! Even DeShlong means well!. And so DO all of those you call "denialists"!
But meaning well does not mean you or even we are seeing clearly. It does not mean that you are somehow different from the rest of humanity in that you can suddenly know the difference between truth and falsehood or are the magic possessor of highest and ultimate truth.
We humans are well proven to have a propensity for seeing only what we want to see, and ignoring anything that even blatantly shows we may be off track. Those you call "denialists" are not your first experience of such, and you yourself and your currently fellow hiv believers are not our first experience of such behaviors in human beings either! We all deal with such behaviors in family, friends, and acquaintances through-out our lives.
And it won't take you long to understand that such behavior is also at the very core of addictions such as drug and alcohol or any other addiction. The recent bank and economical failures, and many other blatant human problems are clear evidence of the quite often inability of us humans to clearly see reality or to see what is not really there!
I freely admit this. The ones you gotta watch are those who DO NOT admit they could be wrong. You yourself are currently in such a position. And getting deeper all the time! Are you really so sure you are right? Are you really so sure the clear evidences that you think are there are actually THERE?
You tell me! You are the one who has lately been searching for it high and low!
I went through all that years ago, and it landed me where I now am perceiving reality from!
As a believer in evolution, I myself would very much like to see us all evolve further than we currently have. But if we do not question ourselves and our preprogrammed beliefs or question the beliefs of others, then this next evolutionary step becomes impossible.
I myself used to be a full believer that hiv was the cause of aids. I didn't question it at all. It took me years of investigating, re-investigating, confirming, and re-confirming and going back and forth and back again, until I myself became fully aware that my own preconceived beliefs had way too many holes to be able to hold water!
And it seems to me that this is also going on not just internally in a few individuals, but also on a societal and global level as well. And THIS, poods, is evolution.
So please, don't struggle so hard. I have just shown you ten very intelligent aspects that must be fully answered in order for hiv theory to hold water. Hopefully, after months and months of your back and forth on this, hopefully at this point you yourself can see the great difficulty you have in finding fully reliable evidences and facts to back up the evidence.
Now, you are welcome to beat your head against a wall all you want, but it doesn't seem to be changing anything, now does it. You still have been unable to clearly demonstrate anything at all!
I realize you like to drink once in a while, but hopefully you have not deadened so many brain cells that this quandary you are in, in attempting to solidify your belief in hiv, is escaping your own notice.
Is it?
Can you evolve yet higher? Can you see the big picture yet? Or does it frighten you too much to even consider such things?
If so, then courage is the doorway. Have the courage to go beyond yourself, Poods. Sometimes, it is possible to do this by saying to yourself "What if?". What if you are wrong? What IF those damn "denialists are right? What if HIV is not the cause of aids? What if I can't prove it is?
Will the world end? Will the sun shine no more? Will you be eternally disgraced? Will you be labeled a "denialist" too?
I realize all of this is very frightening for you. But unless you hold yourself back, you can go farther with all this. You can do it.
We "denialists", who as you also well know all mean well in our own efforts, are even rooting for you!
What you say is very true. Both sides of this argument believe they are right.
Only one side actually is. I suspect that it's the side which has people who actually know what evolution is. As opposed to the mish mash of silly things that aren't evolution that you just called evolution.
That said, I'm interested to hear what answers people have to those 10 questions, if they haven't been answered already. I'm also interested in seeing answers to questions A-D. If your questions are valid then you will only make yourself seem more honest if you pick one of them and answer honestly.
So I take it you won't answer my questions on whether or not you read the paper? Oh you mean you are trying to change the subject? Who would have seen that coming?
"I have just shown you ten very intelligent aspects that must be fully answered in order for hiv theory to hold water."
And these have been answered long ago. However if you choose to lie about reading the evidence and then revert to quoting denialist misconceptions while showing no clear desire to truly learn, what is the point in discussing these "very intelligent aspects" with you?
"Hopefully, after months and months of your back and forth on this, hopefully at this point you yourself can see the great difficulty you have in finding fully reliable evidences and facts to back up the evidence."
The evidence is there, readily available, reliable, and quite clear. My question is why you are so afraid to learn the truth that go out of your way to AVOID information? Sure, you could read the papers for yourself. Hell, if you had any honest questions about things you didn't understand while reading it many of us here would be happy to explain it to you. Instead you hide behind dishonest claims of having read and understood the material while sticking your head in the sand and quoting people who, like you, have obviously not read any of it.
So I ask yet a third time:
Did you:
A) Read it and simply lack the understanding
B) Read the paper but skip roughly half of it
C) Read the paper, understand it and outright lie
D) Not read it at all.
There is much more to the paper than you have read about in denialist websites. Think of this (and I say this not as an insult but rather as something to seriously consider):
Up to at least 2 days ago you were under the impression that
1) Montagnier did not use adult cells, only cord blood cells and
2) that the RT activity could be cell DNA polymerase activity but had no clue that Montagnier ran controls to test for this.
All this was clearly obtained from denialist postings (in fact I found some of your post word for word on other sites) but clearly the paper was not read.
So here is what you should seriously consider: If the sources of information you hold so dear have lied to you in these two instances (and these are from only one paper and on two pretty major points) what else could you be misunderstanding due to denialist sites that you take at face value with no further research?
Poods, dear dear overzealous desperate Poods,
In this interview,
http://www.virusmyth.com/aids/hiv/dtinterviewlm.htm
Montagnier HIMSELF points out the very reasons why the study you present as evidence is NOT sufficient to evidence a retrovirus:
I really loved his quotation "IT IS A REAL SOUP!"
Interviewer: With what did you culture the lymphocytes of your patient? With the H9 cell line?
Montagnier: No, because it didn't work at all with the H9. We used a lot of cell lines and the only one which could produce it was the Tambon Iymphocytes. (12)
Interviewer: But using these kinds of elements it is possible to introduce other things capable of inducing an RT and proteins, etc..
Montagnier: Agreed completely. That's why finally we were not very ardent about using immortal cell lines. To cultivate the virus en masse - OK. But not to characterise it, because we knew we were going to bring in other things. There are MT cell lines which have been found by the Japanese (MT2, MT4) which replicate HIV very well and which at the same time are transformed by HTLV. So, you have a mix of HIV and HTLV. It is a real soup.
DT: What's more it's not impossible that patients may be infected by other infectious agents?
LM: There could be mycoplasmas...there could be a stack of things. But fortunately we had the negative experience with viruses associated with cancers and that helped us, because we had encountered all these problems. For example, one day I had a very fine peak of RT, which F. Barre-Sinoussi gave me, with a density a little bit higher, 1.19. And I checked! It was a mycoplasma, not a retrovirus.
prove it, thank you for that interview. It does not support your position. I suspect you don't know enough to even understand what he IS saying.
The "It is a real soup" quote is where he is talking about cell lines he decided NOT use to characterize HIV, and why.
In the last part he disposes of your mycoplasma/other agents argument, by pointing out that they learned how to handle those issues with cancer viruses - and then giving an example showing that they DID distinguish mycoplasma RT activity from HIV RT activity.
Do you understand any of this stuff?
First, we were discussing the endogenous issue. Second yu ahve just shot yourself in the foot. The RT activity found that particular time was found at a higher density and Montagnier obviously checks his results. You have successfully argued yourself OUT of the contamination issue for that paper by showing why controls are important and that Montagnier did in fact run them due, having had "encountered all these problems".
This however does not negate the fact that you have thus far refused to comment on your lack of reading the paper and your apparent lie to the contrary. Why continue to change the topic? And if you are so confident that you are right, why would you need to lie about such a thing? Finally if you lied about that why should anyone take the time to "debate" you?
Furthermore, you are cherry picking quotes again while ignoring the rest (why would an honest person have to do that?) Lets look at some of the rest of the interview, for example how he knew it was a retrovirus:
"...it is not one property but the assemblage of the properties which made us say it was a retrovirus of the family of lentiviruses. Taken in isolation, each of the properties isn't truly specific. It is the assemblage of them. So we had: the density, RT, pictures of budding and the analogy with the visna virus. Those are the four characteristics.
Or how he could tell it wasn't an endogenuos retrovirus:
"Because we could "pass on" the virus. We passed on the RT activity in new lymphocytes. We got a peak of replication. We kept track of the virus. It is the assembly of properties which made us say it was a retrovirus. And why new? The first question put to us by Nature was: "Is it not a laboratory contamination? Is it perhaps a mouse retrovirus or an animal retrovirus?". To that one could say no! Because we had shown that the patient had antibodies against a protein of his own virus. The assemblage has a perfect logic! But it is important to take it as an assemblage. If you take each property separately, they are not specific. It is the assemblage which gives the specificity.
"At the density of 1.15, 1.16, we had a peak of RT activity, which is the enzyme characteristic of retroviruses.
and
"..in my opinion it was very clear. It could not be anything but a retrovirus in this way. Because the enzyme that F. Barre-Sinoussi characterised biochemically needed magnesium, a little like HTLV elsewhere. It required the matrix, the template, the primer also which was completely characteristic of an RT. That was not open for discussion. At Cold Spring Harbour in September 1983, Gallo asked me whether I was sure it was an RT. I knew it, F. Barre-Sinoussi had done all the controls for that. It was not merely a cellular polymerase, it was an RT. It worked only with RNA primers, it made DNA. That one was sure of.
So I ask a 4th time:
Did you:
A) Read his paper as you claimed and simply lack the understanding
B) Read the paper but skip roughly half of it
C) Read the paper, understand it and outright lie
D) Not read it at all.
Poods, your desperation is betrayed so well in your post above.
But in Luc Montagnier's own words, regarding this early paper, he himself says it best:
Interviewer: When one looks at the published electron microscope photographs, for you as a retrovirologist it is clear it's a retrovirus, a new retrovirus?
Montagnier: No, at that point one cannot say. With the first budding pictures it could be a type C virus. One cannot distinguish.
Interviewer: Could it be anything else than a retrovirus?
Montagnier: No.. well, after all, yes .. it could be another budding virus.
(lets repeat that in case you missed it)
Interviewer: Could it be anything else than a retrovirus?
Montagnier: No.. well, after all, yes .. it could be another budding virus.
Interviewer: Why no purification?
Montagnier: I repeat we did not purify.
(SAY WHAT!!!)
Montagnier: I repeat we did not purify.
(HE DID NOT PURIFY IT???)
Montagnier: I repeat we did not purify.
Montagnier: I repeat we did not purify.
Montagnier: I repeat we did not purify.
Montagnier: I repeat we did not purify.
Montagnier: I repeat we did not purify.
Poods, lets fully admit, as verified above, that even Montagnier himself has presented plenty of reasons to doubt his own study.
But lets ignore that major crack in the foundations, and lets pretend for a moment that this early study is somehow sufficient evidence to believe that the probability of evidence pointed to an exogenous retrovirus.
Is this sufficient evidence to verify causation?
Montagnier would be the first to tell you it does not.
Is this sufficient evidence to claim that T-cells were being killed by it?
Montagnier, who could barely keep any t cells alive with or without a retrovirus, would be the first to tell you it does not.
Is it sufficient to call it the cause of AIDS?
Again, Montagnier himself would say no.
Was it sufficient to declare that the antibodies found in patients who perhaps harbored such a retrovirus, providing there actually was one, be sufficient to determine that those antibodies when found in other patients sera, were caused ONLY by that single presumed retrovirus?
Certainly NOT!
Was any of this sufficient evidence to recommend just 3 short years later that the highly toxic DNA terminator AZT, that had been trialed for only a few months while evidencing a high number of those taking it died or needed blood transfusions to survive, that such a drug should be given out en masse in exceedingly high dosage to the frightened general public that evidenced such antibodies?
Still seems to reasonable minds that Cooler's question about using any such studies to support the use of AZT or any toxic drug, to do anything but treat actual presenting opportunistic infections, remains valid.
Did anyone else back up Montagniers work by purifing this retrovirus or by EMs taken of any patient blood sera?
Not to this very day has such replication with back-up ever been done.
This is pretty interesting quote, Montagnier says the virus was so difficult to isolate, because there was barely any virus,and they didn't think it was the cause! NO wonder Gallo and Levy could only isolate HIV in less than half of patients, and had to rely on antibodies.
DT: Why do the EM photographs published by you, come from the culture and not from the purification?
LM: There was so little production of virus it was impossible to see what might be in a concentrate of virus from a gradient. There was not enough virus to do that. Of course one looked for it, one looked for it in the tissues at the start, likewise in the biopsy. We saw some particles but they did not have the morphology typical of retroviruses. They were very different. Relatively different. So with the culture it took many hours to find the first pictures. It was a Roman effort! It's easy to criticise after the event. What we did not have, and I have always recognised it, was that it was truly the cause of AIDS. (3)
Prove It,
Who said anything about him purifying the virus in his first paper? Aside from the fact that you are the only one claiming this you seem to be doing more cherry picking:
When he said:
"No, at that point one cannot say. With the first budding pictures it could be a type C virus. One cannot distinguish."
Note the "AT THAT POINT". You are ignoring everything except those little bits and pieces that you think will support your point of view.
When asked:
Without going through this stage of purification, isn't there a risk of confusion over the proteins that one identifies and also over the RT which could come from something else?
He responds with:
No .. after all, I repeat if we have a peak of RT at the density of 1.15, 1.16, there are 999 chances out of 1,000 that it is a retrovirus. But it could be a retrovirus of different origin. I repeat, there are some endogenous retroviruses, pseudo-particles which can be emitted by cells, but even so, from the part of the genome that provides retroviruses. And which one acquires through heredity, in the cells for a very long time. But finally I think for the proof - because things evolve like molecular biology permitting even easier characterization these days - it's necessary to move on very quickly to cloning. And that was done very quickly, as well by Gallo as by ourselves. Cloning and sequencing, and there one has the complete characterization. But I repeat, the first characterization is the belonging to the lentivirus family, the density, the budding, etc.. the biological properties, the association with the T4 cells. All these things are part of the characterization, and it was us who did it.
What part of this is unclear to you? Guess what, the sequence in fact confirmed a lentivirus. Guess what else? THERE ARE NO ENDOGENOUS HUMAN LENTIVIRUSES. I don't know how often this needs to be repeated for you to get it.
"Did anyone else back up Montagniers work by purifing this retrovirus or by EMs taken of any patient blood sera? Not to this very day has such replication with back-up ever been done."
Is this coming from your same sources as the ones that told you Montagnier never used adult cells? Read the actual papers instead of filtered out, second hand garbage.
Now will you ever get to answering whether you ever actually read the paper? Why the hell would anyone give any credence to any of the BS you cherry pick/misinterpret/misunderstand/outright lie about if you can't even read what you believe you are discussing?
Again, did you:
A) Read his paper as you claimed and simply lack the understanding
B) Read the paper but skip roughly half of it
C) Read the paper, understand it and outright lie
D) Not read it at all.
And as it is believed that the said guilty retrovirus is ONLY TRANSMISSABLE in LESS THAN 1 in 1000 sexual encouters with any presumed infected individual,
would you care to explain just how such a retrovirus has ever survived in nature?
How many acts of sex have you had in your entire life? Have you had several thousands of sexual encounters that could assure the retrovirus of passing on if you had it? Do you know anyone who has?
If so, how could it have survived in nature for enough generations to allow for it to have been passed recently to the very very very few individuals who have been blessed with such a high natural libido to be able to have even made it possible for them to acquire it and pass it on through sex?
Do you also believe in ghosts and boogeymen and ufo's and space aliens as well? I hear several pictures proving these things exist?
Maybe a ghost mated with a boogeyman in some far away planet, and this caused the retrovirus to come into existence, and then the ghost had an infected teat fed baby who became an alien, built a spaceship, and came down to earth and mated with a monkey who some starved african ate, and then he butt pumped some gay boy who liked dark meat and now it is spreading rampantly, but just to blacks and gays, especially if they are drug abusers.
Well, that clearly explains it. Undoubtedly it all must be true! After all, we have sufficient evidence found in the pictures of ghosts and aliens (who by the way all look like they are suffering from aids), and we have the picture proofs of their spaceships, and I know a few gay guys that like chocolate. They say, once you go black you never go back.
There we go.... Mystery solved..... Poods of course, was right all along!
Prove It,
Please try not to change the subject so quickly as it is clear you have yet to grasp even the smallest bit of the previous discussion. Furthermore, until you answer that one very simple question:
did you:
A) Read his paper as you claimed and simply lack the understanding
B) Read the paper but skip roughly half of it
C) Read the paper, understand it and outright lie
D) Not read it at all.
I see no reason why anyone would believe any of your claims, be they numbers, statistics, or statements of biology. Just answer that question. Why would you lie about such a thing and why should anyone believe anything you claim when you are so obviously incapable of not only admitting when you are wrong, but also telling the truth when it doesn't fit your faith in denialism?
Poods, His statement that YOU think proves or clarifies something, clearly brings up yet another black hole:
"And which one acquires through heredity, in the cells for a very long time".
Clearly indicating the very great possibility that whatever was found was a natural part of that individuals hereditary make-up, and that this hereditary feature, unique to a percentage or so of individuals, was sufficient for evidence and may very well be what was cloned or what caused the antibody responses. Who knows? Surely not he and even more surely not you.
Regarding his statement: "I think for the proof - because things evolve like molecular biology permitting even easier characterization these days."
He seems to be indicating that unsubstantiated indirect and unverified evidences that were used, like RT and PCR were sufficient, simply because he "thinks" they are.
They are not sufficient, as has been often demonstrated, and are proven to often be unreliable.
You can plead and whine and cry and scream and bang your head on the wall. This still does not fill in the gaping holes he himself has clearly presented.
By the way Poods, you seem to be repeating yourself ad nauseum, repeatedly asking questions that I answered long ago.
Does it bother you when someone seems to be ignoring you?
I don't know why it should when you are a pro at ignoring others responses or changing the subject when confronted.
But do keep asking, so I can continue to give you a dose of your own, when I did in fact answer your droning questions quite directly many responses ago!
By the way, Poods, notice again that you have not answered even a SINGLE question that I have asked of you. Not one. But keep demanding, I am sure to come around sooner or later and repeat what I have already answered just to keep you from harming yourself in frustration, but not before you are ready to answer any of the direct questions that I have already asked of you.
Matter of fact Poods, this inability of your to read or understand plain english, seems to be an ongoing problem for you.
My very clear and concise answer to your question, that you have repeatedly and obnoxiously pretended has not been answered is found in black and white, many many posts ago:
http://scienceblogs.com/aetiology/2008/12/christine_maggiore_dies_from_…
And as for my ability to comprehend what I read, it seems to be better than your own comprehension, as you did not comprehend even the 3 letter word of YES.
Furthermore, and not to brag, but I have a sufficiently high IQ to comprehend what I read, and likely it is higher than yours because I do comprehend 3 letter words such as "YES".
So enough of your droning on repeatedly asking the same question that I clearly and concisely and directly answered.
And now, to make up for your false accusations, you can make up for it by answering, without changing the subject, and clearly and concisely, absolutely EVERY SINGLE QUESTION that I posed directly TO YOU, ever since that post!
Because YOU have not answered a single one of them.
"And which one acquires through heredity, in the cells for a very long timeâ Clearly indicating the very great possibility that whatever was found was a natural part of that individuals hereditary make-up, and that this hereditary feature, unique to a percentage or so of individuals, was sufficient for evidence and may very well be what was cloned or what caused the antibody responses. Who knows? Surely not he and even more surely not you.â
Oh my! All this and you bring up the IQ bit, too! Letâs see just how your astronomical IQ helps you out with this. Ready? Try to keep up. I will try to use small words.
The possibility that it was âa natural part of that individuals hereditary make-upâ was already explained. In fact, this is one of the first things done when a new virus is thought to be found. When a retrovirus is âa natural part of that individuals hereditary make-upâ it is called an ENDOGENOUS RETROVIRUS. In humans this is shortened to hERV. Montagnier already explained HOW it could be determined that this was NOT an endogenous retrovirus.
I quoted this above already but in case your enormous IQ is blinding you, let me quote him again:
Because we could "pass on" the virus. We passed on the RT activity in new lymphocytes. We got a peak of replication. We kept track of the virus. It is the assembly of properties which made us say it was a retrovirus.â
Now I donât know if your oh-so impressive IQ can keep up with this but here you go:
1) hERVs are not infectious to human cells and thus could not be "passed on".
2) If they WERE hERVs they would also have been seen in the control (uninfected) cells during the co-culturing. They were not.
3)The retrovirus Montagnier found was a lentivirus both by sequence and morphology. THERE ARE NO ENDOGENOUS HUMAN LENTIVIRUSES!
4) The human genome has been fully sequenced. No endogenous lentiviruses and no HIV.
I realize this may be difficult for you to understand what with that giant IQ and all but tell me if Iâm getting through to you.
âMy very clear and concise answer to your question, that you have repeatedly and obnoxiously pretended has not been answered is found in black and white, many many posts agoâ
Oh yes, you answered that you had read the paper. I have no doubt you said that. My question remains:
A) why, if you had really read it, did you not know that Montagnier used adult cells (especially when roughly half the paper covered their use)? Why did you state that he ONLY used cord blood and only those cord cells were successful? Clearly this was not the case.
and B) Why did you also have no clue as to the controls they used to determine that the RT activity was not normal cellular DNA polymerase?
This is what you havenât made clear. This is why I keep having to ask you this over and over. So why was this? Did you simply not read the ½ of the paper that talked about adult cells or did you lie about it? Did you read simply not read where in the paper he described his controls or lie about that?
Answer to A and B:
Very simple. Because I was referring to THIS:
Montagniers original work in May 1983, in Science vol 220, pp 868-871
Have you read it?
Do you understand it?
Can you comprehend it?
Cord blood.
"Answer to A and B:
Very simple. Because I was referring to THIS:
Montagniers original work in May 1983, in Science vol 220, pp 868-871"
Funny that is the exact same paper to which I was refering. Cord blood and Adult blood cells. If you had read it how could you NOT know this?
"Have you read it?" Yep which is how I know they also used adult cells.
"Do you understand it?" See previous.
"Can you comprehend it?" See previous.
"Cord blood."
Oh and here I thought you were on a roll. WRONG! Cord blood AND Adult cells. Again, how could you not know this if you truly read the paper?
Of course, if you only read the abstract (which doesn't mention the adult cells) instead of the full paper I can see how you would get that wrong idea. Is that what you did? Did you just read the abstract and then lie and say you read the whole paper? I may not have your gargantuan IQ but this seems the most likely scenario.
ROFL! Poodle stomper once again makes you look stupid. It must start to get to you at some point right?
The core question here, is this study enough to prove an endogenous retrovirus?
Now, no doubt, Poodles answer to the above question, would be that he fully agrees with Doctor Peter Duesberg, in finding that hiv is sufficiently isolated, via cloning, to sufficiently verify that HIV is isolated well enough.
Any way you look at it, Montagnier himself, (along with the Perth Group, and other), has clearly shown where several leaking holes are quite possibly located: use of RT, EM's, a real soup, never purified, several other unknowns, etc.
Therefore, it cannot be declared as anything close to a 100% proof of isolation of exogenous retrovirus, and those who disagree with Poodle and Dr. Duesberg's and Montagniers and Gallo's findings still have highly valid reasons to do so.
As all here well know, there are many who still will say, "Insufficient Evidence", and with sufficiently reasonable cause to do so.
So, it would seem to be somewhat of a stalemate at the moment, with Poodle Stomper in agreement with Dr. Duesberg, and Montangnier et al, and Gallo, as having reasonable enough evidence to continue to the next question
I will however, pass this one to Poods, and say, with reservations, that he has evidenced with a reasonable evidence, that perhaps there actually is quite possibly an endogenous retrovirus evidencing itself here.
Now for the next evidences, where is the clear cut evidence proving that this retrovirus, IF it is indeed isolated, causes immune suppression, causes T-cell loss, is reliably the only factor that causes the antibody tests to spring,or is sexually transmitted?
Poodles and Company, as you have taken on the challenge to prove to a high degree that the "denialists" are wrong, please pick any of the above, and we are ready to look at your "clear cut evidences", when you are!
I declare FOUL and lodge a PROTEST of The Referee's finding for PoodleTwats!
As you, "The Ref" clearly points out, this is not anywhere close to 100%, and may damn well be as low as 10% evidence. Where are the EM's from any supposedly infected individual? Nowhere! You admit RT is insufficient, you admit a soup of who-knows-what, and you admit there are still other unknowns! And as for cloning, WHO KNOWS WHAT WAS CLONED?
Unacceptable finding for Poods and Duesberg and Montagnier, and FOUL FOUL FOUL.
All of this still proves nothing!
"I will however, pass this one to Poods, and say, with reservations, that he has evidenced with a reasonable evidence, that perhaps there actually is quite possibly an endogenous retrovirus evidencing itself here."
Sigh, there really is no reading comprehension here at all. All the evidence has shown that the virus Montagnier observed was NOT endogenous but rather thus EXOGENOUS.
"Now for the next evidences, where is the clear cut evidence proving that this retrovirus, IF it is indeed isolated, causes immune suppression, causes T-cell loss, is reliably the only factor that causes the antibody tests to spring,or is sexually transmitted?"
Being that thus far all we have had from the denialist side is distortions of truth, outright lies, and claims based on lack of understanding/reading of the material, why bother continuing to explain these things if denialist sites are the only sources of information you trust? By this point I think any reader here can see just what kind of science denialists are using.
Protest noted, however, I have made and hereby sustain my findings for the camp of Poodle Stomper, Montagnier, and Duesberg et al, only as having "sufficient evidence to pursue it further".
My decision for the first round is finalized.
This one goes to Poods (by a narrow margin and with noted reservations as stated in the above declarative post).
You can either Accept it, Mr. Prove It, or go pound sand!
Yours,
The ref
Poodle Stomper,
While I truly DO most duly THANK YOU for correcting my error of endogenous, as you have shown evidentiary supoort for an exogenous, not endogenous, retrovirus, (though it may have been a freudian slip), your following comment is more than a bit troublesome....
Matter of fact, I am highly troubled by your statement above,
"why bother continuing to explain these things",
as this seems to be a direct admission by you that you are not able, nor capable of presenting any evidences for supporting your positions, beliefs, or theories.
If such is the case, then the entire debate is here-in forfeited by you and the dissident camp would be declared the full winner of their claim that HIV theory is unsupported by sufficient evidence.
You are currently in the lead, though by a narrow margin. Do you so wish to forfeit this debate to the "denialist" camp at this point?
FINE! I accept it. Congratulations to poodletwit on the first round.
BUT Who cares if hiv is shown to be endogenous or exogenous, or even if it is proven to exist or NOT EXIST?
So if it does exist, POODS, the NEXT QUESTION is far and away the more important.... IS (whatever it was the Montagnier believes he isolated) IS HIV PROVEN TO BE THE CAUSE OF AIDS???
So go for it batboy! Show us "denialists" the PROOF that hiv is the sufficient cause of aids! Show us the "clear cut" evidences!
Show us any T-cells that were killed by it!
Show us some study that proves it somehow causes immune suppression!
And at what point, Ref, is the lack of any studies by Team Virus, to be taken as a forfeit? Just how many years should I have to wait for Poods to present anything before Team Denialist gets the gold?
After all, we have been waiting for the proofs for 25 years! How much longer should we wait? May I suggest 24 hours? That will give Team Virus long enough to nurse their aching heads and take an advil or two and come up with something out of their "mountain of evidence".
Does the Ref agree or not that 24 hours is sufficient for Team Virus to take a break and go to the more important Round TWO and to come up with something showing hiv sis sufficiently proven to cause aids (but only in gays, blacks, or drug addicts)?
How much longer should we have to wait for Poods and company to decide whether or not they forfeit and, if not, to present the evidences and PROVE IT?
No, Mr. Prove It,
24 hours is not sufficient. But 25 years is more than sufficient.
As such, I double any time limit to a maximum of 48 hours, as all involved, (including yourself obviously), need a much deserved break to recuperate from the exasperating Round One.
Therefore.... Evidences for round two by Team Virus and/or Poodle Stomper et al, must be forthcoming within a reasonable time period and posted here no later than April 27th, by 4:00 PM.
Any failure to present reasonable evidences by Team Virus, Poodle Stomper et al, within this more than reasonable 48 hour period shall be taken as a full forfeiture by Team Virus of this debate to Team Rethinker.
The Referee
I see from my above post that I myself really need to proof read, no doubt because I am also exasperated to no end from Round One, and therefore in much need of recovery time myself.
The 48 hour TIME LIMIT for providing Evidences by Team Virus for any continuation to Round TWO is NOT April 27th, but quite obviously April SEVENTH by 4:00 PM.
Prove It,
"FINE! I accept it. Congratulations to poodletwit on the first round."
"BUT Who cares if hiv is shown to be endogenous or exogenous, or even if it is proven to exist or NOT EXIST?"
Good, since you admit that you were incorrect I will ask you the following two questions:
1) If you were incorrect in this, a belief about which you obviously were so certain, what else could you be wrong about if you actually bothered to read the material for yourself rather than simply read denialist versions of it?
and 2) If it took you this long to admit (albeit inadvertently) that you not only did not read the paper but also lied about it, why should I, or anyone else expect any different from you on other subjects? If you are willing to lie, poorly, to make yourself appear correct I have little reason to doubt you would continue to do so.
"So if it does exist, POODS, the NEXT QUESTION is far and away the more important.... IS (whatever it was the Montagnier believes he isolated) IS HIV PROVEN TO BE THE CAUSE OF AIDS???"
This evidence is out there just as the evidence that HIV is not endogenous is out there. The problem is that if you continue to stick your head in the sand and use dishonesty a way to support your faith in denialism I have no illusions that any amount of data could truly convince you. I have no intention of further explaining anything to someone who uses deception as you have.
Ref,
Matter of fact, I am highly troubled by your statement above
"why bother continuing to explain these things""
as this seems to be a direct admission by you that you are not able, nor capable of presenting any evidences for supporting your positions, beliefs, or theories.
Pretty poor attempt at baiting. However, my reason for saying this is the easily verified lying by Prove It. Who would want to bother explaining anything to someone who is so entrenched in denialism that they would outright lie in order to appear correct? I don't think any impartial reader would want to bother with this either. In the end, despite what I consider to be your inevitable claim that the "debate" (not that there truly was one, simply lies on Prove Its part and corrections to those on mine) is forfeit, the readers will be more than capable of determining the merits or lack thereof of Prove It's attempt to deceive.
Poods. You are getting off track again in asking me further questions without having answered even a single question that I have put to you in the last 3 dozen posts.
So try to stay on track here poods. You were given round one, now put your evidence where your mouth is Poodletwit within 46 hours for round TWO!
Though, if you want to continue round one, that's fine by me. You still haven't answered questions about campbell's soup, EM's, "We did not purify", or the reliability of RT. Your "win" of round one is still based in a quicksand of insufficient evidence. But if the ref gives that one to you, OK, I already agreed.
If you want to go back to round one, then begin answering all of the questions I had asked of you, as the question asking game is a two way street!
NEXT!!!!!
Would you please present us with any study that evidences
If you wish to continue round one, answer my previous questions so we can clarify that "evidence of yours truly shows hiv as being properly PURIFIED and also isolated directly from the blood of any of the presumed "infected",
Or, move on to:
2) hiv as proven to be causing harm or death to any CD4 T-cells
2a) hiv as proven to be causing immune suppression
3) hiv as being proven to be sexually transmitted
On the basis of what you have presented in round one, mere RT activity, while failing to answer any questions for clarification, all you have fully verified is the following;
Team Virus/Poodletwits has so far displayed.....
1) Failure to clearly prove the existence of a unique, exogenously acquired retrovirus, HIV, but was given the round anyway.
2) Failure to verify the HIV antibody tests are proof of HIV infection.
3) Failure to prove HIV causes immune deficiency (destruction of T4 lymphocytes) or AIDS.
4) The impossibility of haemophiliacs acquiring HIV following factor VIII infusions.
5) Failure to prove the HIV genome, (RNA or DNA) originates in a unique exogenously acquired infectious retroviral particle.
6) Failure to prove HIV/AIDS is infectious, either by blood, blood products or sexual intercourse.
7) Failure to prove what is called AIDS in Africa or Thailand is caused by HIV or is sexually transmitted.
8) Failure to disprove that AIDS and all the phenomena inferred as "HIV" are induced by changes in cellular redox brought about factors other than a retrovirus.
9) Failure to show that AIDS spreads outside the original risk groups
10) Failure to disprove any of the pharmacological data that do clearly show AZT cannot kill HIV and failure to disprove that AZT is toxic to all cells and causes AIDS.
"So try to stay on track here poods. You were given round one, now put your evidence where your mouth is Poodletwit within 46 hours for round TWO!"
Sorry I'd rather not "debate" anyone who resorts to outright lies to deceive people into buying their point of view. I believe that your actions have made it more than clear to any reader the merits of your arguments. Thank you for at least admitting that there is not proof HIV is endogenous. At least you made some progress there. Feel free to actually research some of your other misconceptions.
By the way, Poods, out of shear graciousness, I will answer your mystery about reading or understanding the paper.
Yes, I did read it, and read it again not too long ago when the Nobel was given to Montagnier and Barre-Sinoussi, but do not have current access to it on this system. As such, I am refuting it by by best memory of what it says and what it was about, and hopefully am not confusing it with other papers, as I have read many of them over just the last few months.
As you are cherry picking it, and posting only blips and clips from it, you are therefore even at greater advantage.
But even so, even not having it in front of me, I have clearly demonstrated various and assorted holes in it. Whether they are enough to give you pause or not, or cause you to think for yourself whether the study presents sufficient evidence, depends only on the thickness of your own skull, and your own ability to comprehend.
And, If you have access to it or know of a link to get it without charges, please do share the link or share the full study conclusions and methods, so all here, not just yourself, can be sure to be on the same page, and so we can all clearly verify its weaknesses or strengths for ourselves.
Prove It,
Sorry no can do. I paid my own hard earned money for that article. I'm not going to distribute copyrighted material.
"As such, I am refuting it by by best memory of what it says and what it was about, and hopefully am not confusing it with other papers, as I have read many of them over just the last few months."
You'll forgive me if I don't take your word for this. I think it is obvious to all that you simply read the abstract and got busted for it, especially when you refused to admit you were wrong. A "sorry I don't have the article, perhaps I am wrong" would have been more believable than your constant insisting you were right, ESPECIALLY if you knew you didn't have the article in front of you. Nice try.
Take what you've learned and move on. You've learned that the virus could not be endogenous; take that as a personal win, having learned something new. Now consider that you might very well be wrong about your other points and go research them on your own.
Best of Luck.
Ummm. What makes you think that the same denialist troll won't be back again in a few months using a different pseudonym and claiming yet again that HIV could be endogenous?
Or even under the same name. Sadly, I have no doubts that he will.
Poodle Stomper has now stated:
"Sorry I'd rather not "debate",
followed by various reasons (or excuses).
If this is indeed Poodle S's last word on this debate, and unless he changes his mind or unless someone else from Team Virus submits sufficient evidences to back the Team Virus/Poodle S's claims that HIV theory is fully supported, by April 7th, 4:00 PM, Team Virus will be declared as forfeiting to Team Rethinker, and TR/Prove It will be declared as debate winner.
Are there are no further evidences presented by anyone wishing to join Team Virus to disprove Prove It/Team Rethinker's claim that "HIV/aids theory is only supported with poor and insufficient evidence?
If not, then Prove It/Team Rethinker will be declared as having won the debate in but one round, with only some evidence for an exogenous retrovirus as having been isolated, and no clear supportive evidence of the HIV theory of causation for aids, or sexual transmission, or harm to T-cells or immune systems.
Poodle Stomper, still time to reconsider? Chris Noble? Srsly? Orac? Tara? Anyone at all?
Are there any other takers or joiners to or from Team Killer Virus to support HIV isolation, causation, sexual transmission, or theory?
Has Poodle Stomper been worn out in Round One, has Team Virus officially dropped out of this debate?
Any efforts to save Team Virus, must please post evidences before April 7th, 4:00 PM.
"Whether they are enough to give you pause or not, or cause you to think for yourself whether the study presents sufficient evidence, depends only on the thickness of your own skull, and your own ability to comprehend"
Bold words from someone who did not even understand something as elementary as GFP. Go study some biology, learn the basics (learn to be truthful for crimminy's sake) and maybe then you will be able to understand all this.
From Dr. Luc Montagnier, Nobel Laureate 2008:
"We can be exposed to HIV many times without being chronically infected. Our immune system will get rid of the virus within a few weeks, if you have a good immune system.â
- Luc Montagnier, 2008 Nobel Laureate for Discovery of HIV, in the documentary âHouse of Numbers,â 2009
House of Numbers
This looks like a great documentary, from the trailer. Team Virus comes off a bit muddled.
Understatement of the last 25 years:
"Team Virus comes up a bit muddled".
Yep, most people who believe in killer ghosts do seem a bit muddled. And the more they demand they are correct, the more muddled they become.
Hey Poods, and the rest of Team Virus, I like the following quote from Skeptico over at Orac's post: "If you can't accept that an idea or theory might be false, then YOU are the closed minded one":
http://scienceblogs.com/insolence/2009/04/on_open-mindedness.php
"We can be exposed to HIV many times without being chronically infected. Our immune system will get rid of the virus within a few weeks, if you have a good immune system.â
- Luc Montagnier, 2008 Nobel Laureate for Discovery of HIV, in the documentary âHouse of Numbers,â 2009
He is saying you won't get AIDS from HIV, unless you already have an (aids) Acquired ImmunoDeficiency Syndrome.
How very circular and strange!
What do you think of his recently videotaped statement Pood-O-twiz?
And the reason I asked, Poods,
"What do you think of his recently videotaped statement Pood-O-twiz?
is because you have presented yourself as somewhat of an expert on the crystal clear clarity of Dr. Montagnier of late ; )
Are you seriously asking people here to comment on a one sentence quote with no context of the discussion or has even what's been asked?
Single sentence quotes with no context is called cherry picking. You should know that. Since this comes from a denialist made video portraying the idiots of the Perth group as authorities in a subject they have never actually had any experience in, I also would not be so quick to jump on this as evidence if I were you. You have a bad history with that.
Perhaps you should go back and do some of your own research for once instead of relying solely on denialist propaganda. Its never too late to start. Good luck.
According to Mr Kalichman, "the problem with AIDS denialism is that people are making testing and treatment decisions based on misinformation and disinformation."
This statement has several inferential possibilities regarding the state of Mr Kalichman's knowledge of the research on retroviruses and immune dysfunctions, many of the latter defined outside the context of AIDS. (e.g. idiopathic CD4 lymphopenia)
BTW, is it "misinformation" to say that HIV doesn't cause Kaposi's Sarcoma?
Anyway, I'm going to try and shine a spotlight into Mr Kalichman's psyche according to my own metric of "mental health", starting with the most wacky and working my way down.
He knows the full spectrum of the possible.
He possesses a bold and audacious faith regarding pharma drugs listed by the PDR as toxic (e.g. nevaripine) - a blind acceptance of institutionalized medicine's infallibility. Even to the extent of excluding the possibility of an informed non-consent based on 1) long term nonprogressors - so-called elite controllers and 2) JAMA-published statistics of iatrogenic deaths which exceed AIDS deaths in US by at least a factor of ten. (Here one can introduce another metric: would this type of "bet" be at least as rational as the bets made using derivative financial instruments that resulted in global economic collapse.)
Saying pharma drugs are always best for someone who tests "HIV Ab" so-called poasitive. This flies in the face of research on e.g. glutathione and "HIV infection".
Finally, the one I can't believe, that he's read all the relevant literature to be able to distinguish "disinformation" from rational re-interpretations of findings by HIV specialists.
Disinformation, of course, is a term right out of, you guessed it, conspiracy reserach
And Poodle Stomper, you too are pulling all of our legs on this "endogenous" thing?
Has it ever occurred to you that an in vitro system may not be a precise model of what's going on within a living organism? Especially when it comes to the RT kinetics - where the rubber hits the road?
Here's something for you right out of the literature:
"In general, laboratory strains of human immunodeficiency
virus type 1 (HIV-1) have markedly different biological
properties than virus recently isolated from an infected
individual. The prototype isolate used in tissue culture
experiments, HIV-l[Lai] (also known as HIV-1IIIB), rapidly
replicates to high titers in peripheral blood lymphocytes
(PBLs) and CD4-positive T leukemia cell lines but not in
monocyte-derived macrophages, readily induces large syncytia in H9 and SupTl cells, and causes cell death. The host range of typical "fresh" HIV-1 isolates is usually limited to PBLs and monocyte-derived macrophages and DOES NOT INCLUDE CD4-POSITIVE T-CELL LINES. Recent HIV-1 isolates commonly exhibit slow replication kinetics and low to negligible cytopathicity and frequently fail to induce syncytia, particularly when recovered from seropositive, asymptomatic individuals." (1)
My God, call me crazy, but it seems we have another reason for informed non-consent: the ordinary meaning of "markedly different". One can even go as far as (gasp) concluding that these "fresh isolates" appear to be ERV-like!
But the mind trembles at the very thought; after all, the Elk Mountain Man has already told us HE can't imagine any pathway in the retro world from endogenous to exogenous.
But I trust that Elkie knows whether or not the cell can as effectively "silence" the transcription of an exogenous retroviral provirus as it can any transposable element. That is, as far as the cell is "concerned", the required biochemistry to maintain genomic stability is the same.
KILLER VIRUS FINALLY BURIED IN CHROMATIN (read all about it)
Thus we wind up with the mundane: its perfectly rational, based on looking at the in-vitro kinetics, to declare Gallo et al's "unique cytopathic variant" capable of "cell-free transmission" to be a laboratory artifact.
1. D S Dimitrov, R L Willey, H Sato, L J Chang, R Blumenthal, and M A Martin; Quantitation of human immunodeficiency virus type 1 infection kinetics. J. Virol. 1993 67: 2182-2190.
"One can even go as far as (gasp) concluding that these "fresh isolates" appear to be ERV-like!"
I tell ya what. How about you explain point by point what in the above paragraph (or even the full paper) makes you think these newly isolated viruses "behave like HERVs". Please, i would really like to know how you jump to such an absurd conclusion. Number these reasons 1 through whatever. Have at it.
I found this interesting Q and A with AIDS "Expert" Dr. Joel Gallant from Johns Hopkins. What a joke the HIV theory is.
Retrovirus confusion
Posted on Aug 16, 2005 Since retroviruses do not kill the cells they infect and actually cause cells to multiply at a faster rate, how could a retrovirus kill the very cell it relies on to survive? That being the case, the idea that the AIDS virus disintergrates the cell seems improbable.
On Aug 16, 2005 Joel E. Gallant, M.D., M.P.H. replied:
The problem is not HIV kills cells. Most of the cells it infects would die a natural death in a few days anyway, and HIV doesn't kill the long-lived cells, such as resting CD4 cells, that serve as reservoirs for latent infection. The reason for the loss of CD4 cells with advancing HIV infection is still not completely understood. The real problem is that HIV uses the machinery of CD4 cells to replicate and to propogate itself.
DT said:
"I would endorse Poodle Stomper's comments here"
Well of course you would endorse him, DT, considering that for many years, you have been encouraging and dispensing and making your living by pushing toxic aids drugs, including AZT, to uninformed individuals, OF COURSE you endorse Poods, and any other nonsense and ignorance that ignores the reality of the multitudes of reasons that people get ill, and might thereby imply that you have been correct in so doing.
By the way, how many of those whose drug treatments have been encouraged by you over the years have died, DT?
Do share!
OK. You are crazy.
Who exactly are you trying to impress with this word salad?
question for cooler, at al:
Diagnostic ELISA and Western blots measure two different things, using different methodologies. What do each measure, and briefly, how do they work? What reagents are used for each ,and how are those reagents acquired? What positive and negative controls are routinely included in each test?
Viral load tests measure something different from either ELISA or Western Blotting. What is measured? There are at least 4 different methods used to measure viral load - what are two of them? Which of these methodologies is sometimes prone to 'false positives," and why is that not a problem for the other methods? What controls are routinely done too identify false positives in a viral load test?
If you don't know the answer to all fo these, hw in the hell do you know whether these tests are 'specific' or valid?
So I take it this is the standard of argument we can expect from the HIV denialists when asked for evidence: "Nyaaah nyaaah, you are paid by bigpharma, you dispense toxic drugs, liar liar pants on fire, fingers in ears, I can't hear youuu!"
I can share, as a matter of fact, as we have recently done the figures in my unit.
Here is a sample from the annualised stats:
1985: 258 patients, 31 deaths
1995: 352 patients, 24 deaths
2005: 431 pateints, 8 deaths (6 were patients presenting late with AIDS who had never taken ARVs)
Do you see a trend developing here in relation to when antiretrovirals became available?
I do, but I doubt if you will, you are so entrenched in denial.
So I take it this is the standard of argument we can expect from the HIV denialists when asked for evidence: "Nyaaah nyaaah, you are paid by bigpharma, you dispense toxic drugs, liar liar pants on fire, fingers in ears, I can't hear youuu!"
I can share, as a matter of fact, as we have recently done the figures in my unit.
Here is a sample from the annualised stats:
1985: 258 patients, 31 deaths
1995: 352 patients, 24 deaths
2005: 431 pateints, 8 deaths (6 were patients presenting late with AIDS who had never taken ARVs)
Do you see a trend developing here in relation to when antiretrovirals became available?
I do, but I doubt if you will, you are so entrenched in denial.
Yes, DT, but I notice you quite intentionally left out the years during which you gave them all AZT.
Do SHARE, and show us the figures of each year from 1987 to 1994, so we can see how many you killed with AZT, as that was the only treatment given during those years.
And while you are listing, show us the numbers for lipodystrophy, and neuropathy from 95 to present!
Based on his delusional revisionist history, you have to wonder whether Michael knew anybody with HIV or anything at all about the disease in the period he obsesses about. Many people decided not to use AZT, many people tried it and couldn't tolerate it, and the dose was lowered in 1990. Yet Michael's psychological need to believe that everyone took AZT and that the dose was lowered when combination therapy was introduced means that he cannot ever accept the reality.
How about PML, Michael? I guess you still want people to get PML the way they did in the good old days! Or perhaps you prefer the Maggiore route, where if you completely avoid any effort to treat and prevent opportunistic infections, you can luck out and die of PCP first. Only none of this is a concern for you, as you're not infected, right?
http://www.journals.uchicago.edu/doi/abs/10.1086/598335
Incidence and Outcome of Progressive Multifocal Leukoencephalopathy over 20 Years of the Swiss HIV Cohort Study
Nina Khanna,1,2,a Luigia Elzi,1,a Nicolas J. Mueller,3 Christian Garzoni,4 Matthias Cavassini,5 Christoph A. Fux,6 Pietro Vernazza,7 Enos Bernasconi,8 Manuel Battegay,1 and Hans H. Hirsch,1,2 for the Swiss HIV Cohort Studyb
1Division of Infectious Diseases & Hospital Epidemiology, University Hospital, and 2Department of Biomedicine, Transplantation Virology and Diagnostic Division, Institute for Medical Microbiology, University of Basel, Basel, 3Division of Infectious Diseases & Hospital Epidemiology, University Hospital Zurich, Zurich, 4Divisions of Infectious Diseases & Laboratory of Virology, University Hospital, Geneva, 5Division of Infectious Diseases, Centre Hospitalier Universitaire Vaudois, Lausanne, 6Division of Infectious Diseases, University Hospital and University of Berne, Berne, 7Department of Internal Medicine, Cantonal Hospital, St. Gallen, and 8Department of Internal Medicine, Regional Hospital, Lugano, Switzerland
Background.We investigated the incidence and outcome of progressive multifocal leukoencephalopathy (PML) in human immunodeficiency virus (HIV)âinfected individuals before and after the introduction of combination antiretroviral therapy (cART) in 1996.
Methods.From 1988 through 2007, 226 cases of PML were reported to the Swiss HIV Cohort Study. By chart review, we confirmed 186 cases and recorded allâcause and PMLâattributable mortality. For the survival analysis, 25 patients with postmortem diagnosis and 2 without CD4+ T cell counts were excluded, leaving a total of 159 patients (89 before 1996 and 70 during 1996â2007).
Results.The incidence rate of PML decreased from 0.24 cases per 100 patientâyears (PY; 95% confidence interval [CI], 0.20â0.29 cases per 100 PY) before 1996 to 0.06 cases per 100 PY (95% CI, 0.04â0.10 cases per 100 PY) from 1996 onward. Patients who received a diagnosis before 1996 had a higher frequency of prior acquired immunodeficiency syndromeâdefining conditions ( ) but similar CD4+ T cell counts (60 vs. 71 cells/μL; ), compared with patients who received a diagnosis during 1996 or thereafter. The median time to PMLâattributable death was 71 days (interquartile range, 44â140 days), compared with 90 days (interquartile range, 54â313 days) for allâcause mortality. The PMLâattributable 1âyear mortality rate decreased from 82.3 cases per 100 PY (95% CI, 58.8â115.1 cases per 100 PY) during the preâcART era to 37.6 cases per 100 PY (95% CI, 23.4.â60.5 cases per 100 PY) during the cART era. In multivariate models, cART was the only factor associated with lower PMLâattributable mortality (hazard ratio, 0.18; 95% CI, 0.07â0.50; ), whereas allâcause mortality was associated with baseline CD4+ T cell count (hazard ratio per increase of 100 cells/μL, 0.52; 95% CI, 0.32â0.85; ) and cART use (hazard ratio, 0.37; 95% CI, 0.19â0.75; ).
Conclusions.cART reduced the incidence and PMLâattributable 1âyear mortality, regardless of baseline CD4+ T cell count, whereas overall mortality was dependant on cART use and baseline CD4+ T cell count.
Srsly,
You ask some compelling questions about the HIV tests. Too bad the HIV theory is a bucket of laughs, Dogs test positive on the HIV test........what a pathetic joke of a test!
. (Cancer Res 1990 Sep 1;50 (17 Suppl): 5628S-5630S Studies with canine sera that contain antibodies which recognize human immunodeficiency virus structural proteins. Strandstrom HV, Higgins JR, Mossie K, Theilen GH. College of Veterinary Medicine, Helsinki, Finland):
Abstract. In a serological survey, using the immunoblotting technique, we found that substantial numbers of dog sera from both normal and diseased dogs, including dogs with neoplasia, reacted with one or more human immunodeficiency virus (HIV) recombinant proteins. A total of 144 dog sera were tested, and 72 (50%) of them reacted with one or more HIV recombinant structural proteins. Ten dog sera were also tested for reactivity with simian immunodeficiency virus (SIV), feline immunodeficiency virus (FIV), and caprine arthritis encephalitis virus (CAEV). Six dog sera reacted with at least the major core protein of HIV, while one of the dog sera tested reacted with SIV core protein, and there were no reactions with the viral proteins of either FIV or CAEV. Cell extracts from canine peripheral blood lymphocytes cocultivated with human cells and an extract of human cells infected with HIV were immunoblotted against dog sera which previously tested positive or negative on HIV recombinant protein commercially available Western blot strips. Two lymphocyte lysates and the HIV-infected Hut cell lysate reacted with the Western blot strip-positive dog serum; however, no reactions were seen with the Western blot strip-negative dog serum."
http://barnesworld.blogs.com/barnes_world/2006/09/darin_brown_exp.html
Cooler,
Have you read and understood this paper or just what denialists have to say about it?
To paraphrase from a movie most of us have probably seen "That paper, I do not think it means what you think it means".
Inspector Clouseau
Does your dog bite?
Hotel clerc
No,Monsieur.
SNAP! The dog bites, Clouseau catches stress and dies soon after from disseminated herpes.
Willingly.
87: 282 (30 deaths) 10.6%
88: 280 (24) 8.6%
89: 301 (22) 7.3% Didanosine & AZT
90: 318 (18) 5.7%
91: 328 (25) 7.6% DDI/zalcitabine/AZT use
92: 333 (22) 6.6%
93: 339 (29) 8.5%
94: 350 (26) 7.4%
95: 352 (24) 6.8% HAART
96: 377 (16) 4.2%
You can see that use of ARVs leads to a decline in death rate among the cohort. We used AZT widely until recently, either as combivir or as trizivir. So the drop in mortality occurred in the face of widespread AZT use.
I have no current figures on lipo, but many of my patients have expressed relief that they are alive and well (except from facial lipoatrophy) rather than dead.
cooler:
"Srsly,
You ask some compelling questions about the HIV tests. Too bad the HIV theory is a bucket of laughs, Dogs test positive on the HIV test........what a pathetic joke of a test!"
Cooler, that is not 'the HIV test." It is not even "an HIV test."
It is the result of a low-stringency screen for cross reacting proteins, and therefore, for evidence that there might be viruses in dogs that are similar to HIV.
Note the part about "low stringency." HIV diagnostic tests for humans are not done at low stringency, and none of those dogs had sera that tested positive on human HIV tests.
That answer, BTW, solidifies my belief that you don't have a fricking clue what you're talking about. Well, I already knew that, but... I note that you didn't bother to answer any of my "compelling questions." I don't think you can.
No you are lying you piddly denialist. Dr. Turner from the the Perth hospital has written a brilliantly eloquent debunking of the HIV test. Are you prepared to bow your head to your scientific father Dr. Turner?
"Writing in the journal Cancer Research, Strandstrom and colleagues reported that 72/144 (50%) of dog blood samples "obtained from the Veterinary Medical Teaching Hospital, University of California, Davis" tested in commercial Western blot assays, "reacted with one or more HIV recombinant proteins [gp120--21.5%, gp41--23%, p31--22%, p24-- 43%]" [4]. Assuming Californian dogs are not infected with HIV (as did the authors) one must conclude these data are further proof of antibody cross reactivity to many of the "HIV" proteins."
http://www.virusmyth.com/aids/hiv/vttests.htm
Cooler,
How many times now have you repeated a denialist line that you read somewhere, been proven wrong and then called the other person a liar to cover up your own ineptitude? In fact, I recall you admitting outright to lying. That would make you a liar AND a hypocrite. Any reason why anyone should believe your uneducated quoting of denialists?
As for Val Turner, he has been judged to bee to ignorant to be an expert witness in court by a judge who said (among other things):
He relies entirely on his interpretation of various studies in the specialized disciplines of virology, epidemiology, microbiology, immunology, pathology or infectious diseases, in none of which he has qualifications beyond his medical degree. He has no practical experience, and has performed no research which has been published.
Bow down to your father Cooler. Truly you have been made in his image!
Poodle Stomper:"Have you read and understood this paper or just what denialists have to say about it?"
Cooler:Posts link to denialist interpretation of paper.
Cooler can you describe figure 3?
"US military service [3], of the 1% or 12,000 who had first time positive HIV ELISAs, only 2000 were ultimately shown to be also WB positive and thus, according to the authors, HIV infected. That left 10,000 positive ELISAs which must have reacted for reasons other than "HIV antibodies", a fitting testimonial to the problem caused by cross-reacting antibodies."
WOW! What a joke the test is! The Elisa is positive but WB is negative WTF? Arf Arf! Dogs test positive? I don't have access to the full paper but what a joke this test is! God poodle stomper is such a low life idiot.
You do in fact: http://cancerres.aacrjournals.org/cgi/reprint/50/17_Supplement/5628s.pdf
It uses sucrose gradient purified HIV, which I think the Perth deniers deny exists.
This is the abstract of the other paper you cited.
N Engl J Med. 1988 Oct 13;319(15):961-4.
Measurement of the false positive rate in a screening program for human immunodeficiency virus infections.
Burke DS, Brundage JF, Redfield RR, Damato JJ, Schable CA, Putman P, Visintine R, Kim HI.
Division of Communicable Diseases and Immunology, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.
In a program screening civilian applicants for U.S. military service for human immunodeficiency virus (HIV) infection, we studied the frequency of false positive diagnoses retrospectively among applicants seropositive for HIV in a subpopulation with a very low prevalence of infection. That subpopulation was defined as consisting of all applicants tested between October 16, 1985, and June 30, 1987, who were young (17 or 18 years of age) and resided in a rural county in a state with a low incidence of reported acquired immunodeficiency syndrome (n = 135,187). Serum specimens from 15 applicants positive for HIV in this low-prevalence subpopulation were retrieved from a serum bank and retested by two Western blot methods, radioimmunoprecipitation, and an immunoassay constructed from a molecularly cloned and expressed viral envelope polypeptide. Fourteen of the 15 samples were unequivocally positive on all retest assays, and 1 was negative. Thus, the measured rate of false positive diagnoses in this program was 1 in 135,187 persons tested. Factors important in achieving a low false positive rate were redundant, multistep testing algorithm, conservative criteria for interpreting Western blots, the requirement that a second, newly drawn serum specimen be tested for verification before a diagnosis of HIV was considered established, and tight quality control of laboratory testing procedures. We conclude that a screening program for HIV infection in a low-prevalence population can have an acceptably low false positive rate.
So, cooler doesn't know how to use Google Scholar.
Cooler, it took me about 30 seconds to get the paper, and most of that was download time.
Figure 3 is clear - the positive control lanes show what a western blot looks like for HIV positive human sera.
Not one of those dogs are 'positive' for HIV, by any criteria used by anyone, anywhere, in scoring an HIV diagnostic western blot.
http://cancerres.aacrjournals.org/cgi/reprint/50/17_Supplement/5628s.pdf
this bear repeating:
"Thus, the measured rate of false positive diagnoses in this program was 1 in 135,187 persons tested."
Read the Discussion. They say that antibodies to HIV specific proteins were found, and in some cases more than one protein, which they say is a specific rather than non specific reaction.
Now if these proteins were unique to HIV the dogs should not have reacted at all period. Arf Arf. Oh, srsly, yes the Western Blot Criteria, where in America you need 3 bands to be positive, Africa you need 2, and in Australia you need 4? What criteria? The get on the plane and change from being on HIV positive and back to negative depending on what country your in criteria?
DT,
Thanks for perfectly proving my point.
My math shows that you ended 1987 with 282 patients, and in less than 3-1/2 years later,....
....JUST OVER ONE THIRD OF YOUR ORIGINAL 1987 count of 282 PATIENTS WERE DEAD!
One more time..... Within 3-1/2 years, DT, ONE THIRD OF YOUR ORIGINAL 1987 count of 282 "patients' WERE DEAD.
Labeled as sexual lepers, then stressed and scared to sickness and death by all of the branding and hyping to them that they were going to die of aids, and then they were finished off by the meds that you, yes you yourself, encouraged.
Nice Job, DT and company!
Quite the life-savers you and your clinicians are! Only 1/3 of the victims, I mean patients, killed off every 3 years or so!
Jumpin Jiminy! That takes almost as much talent as Robert Gallo, but not nearly as good a record as David Ho and JP Moore. They are much more efficient than you, but, who's counting.
Good thing the CDC and aids do-gooders keep hyping the non-specific hiv antibody tests or you would be out of a job in no time.
You poor thing, you and your friends better go stress out a few more victims and hype them some more nonspecific antibody testing before you guys go broke!
But before you do, and as you now seem so willing to make your full public confessional, would you also please share with us how many you and your cohorts have also destined to lifelong disfiguration by lipodystrophy or have ruined their lives with neuropathy, bone loss, lifelong diapers, etc?
Yah know DT, when I see things like the numbers that you posted here,
I am almost speechless. I just absolutely find it so beyond me that seemingly intelligent and caring people such as yourself, can be so absolutely in denial, when your own facts and figures speak such volumes.
The only thing I can possibly think to attribute it to is the amazing ability of human minds to go completely into denial especially when faced with the blatant facts that so clearly show them to be mistaken or wrong. After all, who wants to admit they are wrong. You yourself can clearly see this human behavior almost every day in people you know well or work with.
And just like you yourself, when you are faced with such, I myself just really do not understand how it is possible for you to fail to be capable of seeing the bigger picture and all of what are to me the very clear and obvious links that have nothing to do with any retrovirus.
Is it that you are unable to understand what others are going through? Are you unable to feel or empathize for others? Are you unable to compassionately understand what they are going through? If so, that is classic psychopathology.
How can you, particularly after all of the "patients" you claim to know or have seen, possibly fail to see the common links in their lives?
The link of low self esteem to self abusive behaviors and stress and sickness.
The link of stress to sickness and low t-cell counts,
The link of sickness and low t-cell counts to nonspecific antibody tests,
The link of nonspecific antibody tests to devastatingly more stressful hiv/aids death diagnoses,
The link of devastatingly stressful hiv/aids diagnoses to more self destructive behaviors or worse illnesses,
The link of the diagnoses and subsequent sicknesses to known highly toxic drugs, and m
The link of the combination of ALL of these to deaths.
Just how can any semi-intelligent non-psychopathic person see all of this over and over and over and over, and still not "get it"?
Isn't "not getting it" or not being willing to "get it", the very definition of being in denial?
But then again, denial and psychopathic personality disorders also go hand in hand as well.
And, like an alcoholic being confronted with his/her alcoholism, the very fact that you yourself get so emotionally devastated and angered by the dissidents or by the words of N. Hodgkinson or others, and go immediately into self protection mode decrying your innocence, just exactly like an accused drunk, is nothing but further evidence that you simply don't "get it" because you simply do not want to get it. And are either eyeball deep in denial, or perhaps are a psychopath.
But I suppose if someone did contribute to others pain, suffering, and death, unwittingly or not, then I suppose "not getting it" becomes a mode of self protection. Of the ego trying to protect the self from its own self recrimination if it did accept the obvious.
I mean, after all, what self respecting (or self loathing) alcoholic wants to own up to the devastation and problems he caused by being a drunken fool? None do. No wonder so few go into recovery without coming a hairs breath away from loosing their lives due to their addiction.
I very much see you, DT, in that same light. As well as the multitude of other hiv believers and pushers and do-gooders, who are unwilling to hear the words of the dissidents because it clearly incriminates the do-gooders as having been a major part of the problem, and even as culpable and responsible, for their own part in all of the sickness and deaths that have occurred.
So just know that, DT, that when I converse with you, I consider that I am dealing, not with an alcoholic, but with just another of the many many thousands of hiv/aids-aholics.
Too bad there is not some kind of a 12 step program for them. Though, surely few would go, even if there was.
I suppose ultimately I just feel sorry for you and all the others like you. Reminds me of the words of Jesus, "forgive them, they know not what they do".
I knew it would be a mistake to let a novice loose with data they cannot interpret. To clarify, the numbers of patients refers to the number of living patients, not alive and dead, so the "cohort" size needs to include deaths as a denominator, and by that parameter the deaths as percentage of the total cohort are fewer (22% over the 4 year time frame). Fact is, AIDS can kill, or didn't anyone tell you
But you conveniently ignore the original point of your post - that we are accused of killing patients with AZT.
1. You fail to appreciate or explain why even more patients died before the days of AZT. If it is so toxic, deaths would rise.
2. You have said no other ARVs were in use before 1995 except AZT - that is quite untrue, since several others were in use; we used ddI from 1990, and by by 1992/93 dual thgerapy was standard.
3. You also conveniently forget that AZT was still used widely until very recently -and in fact still is used in some patients dependent upon resistance profiles- Do you think it was withdrawn in 1995? Of course not.
4. You also do not know what any of these patients died from; I have not told you. Most have died from AIDS-related problems, some from totally unrelated factors like assault/accidental death, some from natural causes/other medical pathology, some from end stage liver disease in HCV coinfected patients. None from AZT toxicity, I can assure you, and as far as we can tell, none from other drug toxicities but this is harder to tell as we have had 6 patients die from cardiovascular disease in the last 10 years and this may be indirectly due to therapy (but they all had other CV risk factors). And none died from "stress".
5. You also fail to explain why increasing use of ARVs has reduced the death rate in the cohort, and why the mortality rate significantly declined with the introduction of HAART which included at that time AZT as standard backbone. Oh, I know, perhaps we are causing them "less stress"? Perhaps as they all dissolve into lipoatrophy and get other side effects (your claim) they feel so at peace with themselves and at one with the world that their T cells rise?
Perhaps we can describe a new syndrome, where complex therapies with (according to you) overwhelming toxicities actually act specifically as a potent form of relaxation therapy? Have we found the new reflexology/aromatherapy for the 21st century?
Hmmmm, let me get a calculator, and figure out what Christine Maggiore's life expectancy would have been if she had submitted to aids drug treatments encouraged (demanded, prodded, pushed) by DT and DT's co-clinicians.........
According to DT's own figures, ONE THIRD of all hiv positive patients at DT's clinic died in less than 3-1/3 years.
Let's do some more math. 3-1/3 years X 3 equals 10 year maximum life expectancy. But, Christine Maggiore lived longer than 19 years after being diagnosed, without DT"s AIDS drugs.
This means that if Christine Maggiore, who had been diagnosed as hiv poz had been treated at DT's clinic, Christine would have had a 100% expectancy of being dead ten years ago.
But, instead of dying a virtually 100% garanteed 10 years ago via DT's recommended treatment of DNA terminators, instead, Christine Maggiore refused the poisons, and gave birth at that time to a sweet, beautiful, and also hiv negative son, who himself is now just over 10 years old.
And to top it off, even having lost her daughter, even having been harassed and attacked and painted in media, TV, and blogs, and emails and phone calls as a child killer by DT and friends, even with the stress of all that, and the additional stress of confronting the coroner in court, Christine Maggiore STILL LIVED without DT's "life-extending drugs" for an additional TEN YEARS.
Even with all of that stress (added to by DT and company) Christine Maggiore lived twice as long as DT's aids drug treated patients.
According to this simple and obvious fact, it would be safe to assume that doubting hiv, and joining hiv/aids rethinkers, and becoming an AIDS dissident is hereby verified by Christine Maggiore herself to save and extend lives, far beyond any such life expectancy by using aids drugs.
"Oh, I know, perhaps we are causing them "less stress"?"
WOW DT!!!!
DT's lights suddenly turned on!
You really are brighter than I previously gave you credit for.
Please keep up the good work and continue to cause them less stress.
PS, and by the way.....
you might also consider ending the lifelong chemo and black label drugs, and just treat the presenting diseases instead of phantom boogeymen. A dollar to a donut says you will even increase the current life expectancy, at least for those who still want to live after being branded a sexual leper.
Don't want to address any of the points I made? No, didn't think so. Rational, evidence-based discussion is obviously beyond your abilities.
So how long did Christine survive for following her AIDS presentation? 2 weeks? (at least her AIDS survival exceeded her daughter's) The longest surviving patient in our clinic was originally diagnosed with PCP in 1983. That's 26 years and counting.
1. You fail to appreciate or explain why even more patients died before the days of AZT. If it is so toxic, deaths would rise.
You are lying to yourself again DT, and quite blatantly.
There were far less US aids deaths in 1986 than in 1987 and the years following it when AZT was released. The deaths skyrocketed from the introduction of AZT in 87 until just after doctors began abandoning it in 93/94.
The proof of your lie is obvious, DT.... It is clearly found in the US annual deaths:
http://en.wikipedia.org/wiki/File:AIDS_Deaths-US_1987-1997.gif
Any imbecile (no offense) can look at the graph and clearly see that aids deaths went from less than way less than 10,000 in 1986, and reached 50,000 yearly shortly before AZT monotherapy ended.
Was it ONLY the AZT, of course not.
Every HIV positive was STRESSED TO BREAKING by believing that they were was no hope for them to live. Every doctor and every clinician affirmed to all of them that they would die.
The clinicians and doctors and scientists fully contributed by feeding the stress via diagnoses of inevitable death.
You yourself still continue to project inevitable death by aids, at our society, and to all of your patients, unless they take or comply with taking black label proven deadly toxic drugs.
Try to find some courage to deal with the reality of all of this, DT.
The truth will set you free.
Holy fucknoly! Tara, I thought I had loons at my blog, but they are nothing compared to this shit. What is the motivation for these people to so vehemently delude themselves?
You yourself still continue to project inevitable death by aids, at our society, and to all of your patients, unless they take or comply with taking black label proven deadly toxic drugs.
That's what, six blatant lies in one paragraph? Must be a new record.
The proof of your lie is obvious, DT.... It is clearly found in the US annual deaths:
Any imbecile (no offense) can look at the graph and clearly see that aids deaths went from less than way less than 10,000 in 1986, and reached 50,000 yearly shortly before AZT monotherapy ended.
You know, as strange as this may sound I agree with part of what Mike says here. The average "imbecile" can indeed see that AIDS deaths were going up.
Of course if takes a massive imbecile to not notice that the graph itself starts at 1987 and doesn't cover the period before. It would also take a gargantuan imbecile to not notice that the graph shows only AIDS deaths and not AIDS deaths relative to AIDS diagnosis or HIV infection.
Only a superb "imbecile" would look just at AIDS cases without taking THAT into account...right?
Stop insulting imbeciles here, you can't get to 25 on the IQ test if you keep insisting the round peg goes in the square hole.
"Only a superb "imbecile" would look just at AIDS cases without taking THAT into account...right?", says the pood.
No Pood. What a "superp imbecile" would not take into account, is that aids deaths and aids diagnosis and aids disease, were all pretty much the same thing when it came to AZT, at least according to the PDR:
"It was often difficult to distinguish adverse events possibly associated with zidovudine [AZT] administration from the underlying signs of HIV disease" - Physician's Desk Reference, 1994.
"It was often difficult to distinguish adverse events possibly associated with zidovudine [AZT] administration from the underlying signs of HIV disease" - Physician's Desk Reference, 1994.
Ok, man, and they gave that drug to peeps that tested hiv from 87 to 95? and that drug "often" causes the same symptoms as the disease?
Total wipes dude. Total bottom feeding a-hole wipes. That graph. Dude! They sure killed off a lot gays with that crap.
"The longest surviving patient in our clinic was originally diagnosed with PCP in 1983. That's 26 years and counting."
Wiggling light shades again DT? Good thing your anecdotatal patient wasn't treated by you or your clinic for the first 25 years of his diagnosis, and good thing he didn't believe the likes of you when they told him he would be dead in 3 years, and good thing he also flushed his AZT away, and good thing he didn't take most of his other drugs, and good thing he didn't have the likes of you calling him a child killer all over the internet and tv and phone calls and emails, etc, etc, etc....
"good thing he didn't believe the likes of you when they told him he would be dead in 3 years, and good thing he also flushed his AZT away, and good thing he didn't take most of his other drugs"
Any evidence for any of this other than you wish to discount it simply because it doesn't fit into your little denialist-faith? No? Just more speculation? Ok, I just wanted to make that clear.
So, the resident denialist loons just discovered the dying years. Guys, those tragic years began BEFORE introduction of AZT.
Care to tell us why death rates dropped upon introduction of HAART, which included continued use of toxic AZT, plus the addition of a lot of other toxic drugs in addition?
There are so many holes in your disjointed ramblings I don't even know where to begin. But let's start with your graph.
1. 1986 figures are not given, where do you get these from?
2. The highest recorded deaths are 41,000 in 1995. Where do you get 50,000 from?
3. The year before AZT monotherapy ended was 1990, when deaths were 24,000. When do you think it was, and why do you think it shows 50,000 deaths?
No offence, but if even an imbecile can interpret this graph, what does that make you?
Azidothymidine (AZT) is not very inhibitory to mammalian DNA polymerases. This is why it filed as an anti-cancer drug; it did not inhibit rapidly dividing mammalian cells. It is quite inhibitory to retroviral reverse transcriptases, which is why it rapidly lowers viral loads, protects infants from mother-to-infant transmission, and is very useful in combination with other drugs for long-term therapy.
AZT does seem to inhibit mitochodrial Thymidine phophorylation[1], so damage to mitochodria can occur from long-term use, and patients should have regular check-ups.
Refs:
1) Phosphorylation of thymidine and AZT in heart mitochondria: elucidation of a novel mechanism of AZT cardiotoxicity.
McKee EE, Bentley AT, Hatch M, Gingerich J, Susan-Resiga D.
Cardiovasc Toxicol. 2004;4(2):155-67.
PMID: 15371631
You all realize that you will not be able to convince any of them they have been fooled. The dellusion they suffer from stems not from a belief they are right but from a very deep seated need to be different.
Believing that there is a worldwide conspiracy to poison millions of people, and that they are the only one's that know, satisfies an intense craving to demarcate themselves from the middling crowd araound them. And their crusade to convince others that they, and only they are entrusted with the truth, feeds their heroic self fantasies.
Had they not latched on to HIV denial, they would be fighting the egyptodoxy, claiming there is a secret code engineered into the dimensions of the pyramids, or that Atlantis is out there under the Atlantic ocean waiting to be found, that the Moon shots were a hoax perpetrated by an evil Government on a gullible people or like a man I once met who claimed that J.F.K. was assassinated by use of a jelly bean spider. Every once in a while the institute would let him out for a stroll and a coffee.
By the way, if any of the more scientifically minded amongst know what a jelly bean spider is...
What makes you think that these are mutually exclusive?
Cooler is a 911 troother.
I'm not sure about his thoughts on the moon landing or the JFK assasination.
Ah, the great defenders of the faith. So sorry I've been missing your grand diatribes, rants and phoney baloney over here. But.. I got to hand it to you at least your persistent.
Question: If Luc Montagnier says, " We can be exposed many times to HIV without having been infected and our immune system can get ride of the virus in a few weeks if you have a good immune system", wouldn't that mean that HIV is a result of immune deficiency and not the other way around as we've been forced fed to believe?
Chris
People who buy into AIDS Denialism are prone to conspiracy thinking. We all know that. What is fascinating is that those who propagate AIDS Denialism display a mix of paranoid and narcissistic traits â a pretty dangerous combination. It is that paranoid grandiosity propelled by an insatiable need for attention that we see in every single one of the major AIDS Denialists. They crave attention. Why do you think this thread is alive and well four months after Maggiore is dead and gone?
Seth Kalichman
http://denyingaids.blogspot.com
Chris, can I ask some questions? How many civilians died in the Vietnam war? Was Vietnam a threat to the National security of the United States? Chris can you explain and justify Operation Northwoods? Did the Iraqi government really throw babies out of incubators, or was this war propaganda that led to the deaths of millions of people? Were there WMD's in Iraq? Are you stupid?
Carter, I believe this has already been addressed.
In short you are getting all excited about a two sentence quote with no given context and with the question posed being unknown (at least from the clip available on the house of cards" site).
This is cherry picking and not at all surprising coming from denialists as it seems to be the norm.
Perhaps if you supply the full conversation, context and questions, things will be more clear.
Exactly Montagnier's quote defies the common wisdom about HIV, once HIV replicates in your body it's over according to the othordoxy, the official reasons people don't get infected is because the virus never enters them, which is why certain sex acts (anal sex) are considered much more risky than others.
This is not suprising at all, Montagnier has stated several times in the early 90's that HIV was harmless without other factors. There is a great article called "IS hiv Guilty" from the Miami Herald where he and many other scientists doubt HIV. I'm glad Montagnier seems to have the integrity to speak out again.
And srsly, the death rate dropped possibly because they lowered the dosages of AZT. Since most every aids drug is not tested against placebo, including the cocktails it's pretty crazy for you guys to say how effective they are without any evidence.
Cooler,
"the official reasons people don't get infected is because the virus never enters them"
What is your source for this?
"And srsly, the death rate dropped possibly because they lowered the dosages of AZT."
Any evidence for this "possibly" or are you pulling stuff out of your ass again?
"his is not suprising at all, Montagnier has stated several times in the early 90's that HIV was harmless without other factors."
Source?
You realize that you've said so much BS that was 99.99% of the time completely incorrect/misunderstood/lies that unless you cite some credible evidence for this I don't think anyone will give it a second though.
Also
"Exactly Montagnier's quote defies the common wisdom about HIV, once HIV replicates in your body it's over according to the othordoxy"
Please look up something called "minimal infectious dose". It may help you understand a little more about why your above statement is complete BS (again).
"There are too many shortcomings in the theory that HIV causes all signs of AIDS," says Luc Montagnier.
http://www.virusmyth.com/aids/hiv/ebhiv.ht
Is HIV Guilty Miami Herald 1990
âThere are too many shortcomings in the theory that HIV causes all signs of AIDS. We are seeing people HIV-infected for 9, 10, 12 years or more, and they are still in good shape, their immune system is still good. It is unlikely that these people will come down with AIDS later.â
âHIV is neither necessary nor sufficient to cause AIDS.â
VI Intâl AIDS Conference, Jun 24 1990
â[Luc] Montagnier said clearly what he meant. HIV is a necessary but not, without the cofactor, a sufficient cause of AIDS.â
Nature 1992, 357:189
â John Maddox, Editor, Nature Magazine
Are you stupid? What evidence do you have the Haart reduced deaths retard? Since none of these drugs are tested against placebo( except for the crooked AZT trials) or in animals it very telling how you accept their "success" without any evidence.
What is your source that people get infected with HIV and are told their immune system can defeat it? That would mean someone injected with HIV would have a good chance to beat it? Is that what the orthodoxy has been telling us? Why do they say anal sex is the most risky? Isn't that because it allows the virus the easiest access to the bloodstream?
How much of a lying low life can you be? Are you so scientifically illiterate that you don't know Montagnier said "HIV might me benign" at the 1990 AIDS conference 3 years after AZT was approved? Even the Editor at Nature realized this. I swear you are totally pathetic.
I've seen the film in it's entirety and I read you no answer, answer previously. So what gives? Can't you or you cohorts answer a simple question?
I have never believed that the Iraq war was justified. That doesn't mean that I believe the ridiculous paranoid conspiracy theories about a controlled demolition of the WTC. Don't try to impose a false dichotomy.
Any comments on JFK and the moon landing?
Cytotoxic T cell responses to multiple conserved HIV epitopes in HIV-resistant prostitutes in Nairobi. J Clin Invest. 1998 November 1; 102(9): 1758â1765.
Carter,
"I've seen the film in it's entirety and I read you no answer, answer previously. So what gives? Can't you or you cohorts answer a simple question?
First, I'm not sure what you mean by "I read you no answer, answer previously". To answer "Can't you or you cohorts answer a simple question?" the answer is, without knowing the context of the answer or even what question was asked, the best we can do is take an educated guess.
So you watched the movie? Tell me what the rest of his quotation linked to this was. Tell us the context and the question asked.
Cooler,
In the early year of HIV research there were many who postulated the need for a co-factor. Montagnier was one, Robert Root-Bernstein was another. Let me ask you this. What do they believe now that further research has been done? Do you simply copy and paste denialist web sites without thought or have you looked into how their views might have changed after almost 19 years of research? If I show you that Montagnier changed his mind since those very early days, would you still believe him to be worthy of being quoted as an authority or will you claim he changed his mind so he doesn't get Duesberged?
Unheard of!! Only went back as far as 2003, then started to get worried about carpal tunnel syndrome from all the cutting and pasting.
Suggested search term: "HIV exposed seronegative"
AIDS. 2009 Jan 14;23(2):161-75.
The 'immunologic advantage' of HIV-exposed seronegative individuals.
Miyazawa M, Lopalco L, Mazzotta F, Lo Caputo S, Veas F, Clerici M; ESN Study Group.
AIDS Res Hum Retroviruses. 2008 Nov;24(11):1415-27.
Impaired viral entry cannot explain reduced CD4+ T cell susceptibility to HIV type 1 in certain highly exposed individuals.
Speelmon EC, Livingston-Rosanoff D, Desbien AL, Lee J, Wick WD, Hladik F, McElrath MJ.
Medical Scientist Training Program, University of Washington, Seattle, Washington 98105, USA.
Rare individuals report repeated unprotected HIV-1 sexual exposures, yet remain seronegative for years. We investigated the possibility that reduced in vitro CD4(+) T cell susceptibility to HIV-1 infection protects such highly exposed seronegative (ES) individuals. Susceptibility to three R5-tropic HIV-1 isolates, regardless of inoculating dose, was remarkably similar between 81 ES and 33 low-risk controls. In 94% (99/105) of donors, we observed a 1.36 log-unit range in HIV-1(JR-CSF) production, with similar results for HIV-1(1192). The median frequency of intracellular Gag(+) T cells after single-round infection was similar in ES (5.2%) and controls (7.2%), p = 0.456. However, in repeated testing, CD4(+) T cells from two controls (6.1%) and four ES (4.9%) exhibited a 10- to 2500-fold reduction in HIV-1 production and required 5- to 12-fold greater HIV-1(1192) and HIV-1(JR-CSF) inocula to establish infection (TCID(50)). Reduced viral entry cannot explain the low producer phenotype; no differences in CCR5 receptor density or beta-chemokine production were observed. In conclusion, we have identified a remarkably narrow range of HIV-1 susceptibility in seronegative donors regardless of risk activity, which can be applied as a benchmark to assess vaccine-induced antiviral effector activities. However, CD4(+) T cells from a subset of individuals demonstrated reduced HIV-1 susceptibility unexplained by impaired entry, lending support to the possibility that cellular restriction of HIV-1 may account for continued seronegativity in some of those having repeated sexual exposure. Identifying the host-virus interactions responsible for diminished in vitro susceptibility may contribute to the development of novel therapeutic strategies.
Curr HIV Res. 2008 Nov;6(6):531-8.
Increased levels of human beta-defensins mRNA in sexually HIV-1 exposed but uninfected individuals.
Zapata W, Rodriguez B, Weber J, Estrada H, Quiñones-Mateu ME, Zimermman PA, Lederman MM, Rugeles MT.
Group of Immunovirology, School of Medicine, University of Antioquia, MedellÃn, Colombia.
Protection against HIV-1 infection in exposed seronegative (ESN) individuals likely involves natural resistance mechanisms that have not been fully elucidated. Human beta defensins (HBD) are antimicrobial peptides found primarily in mucosae, the main ports of HIV entry. HBD-2 and 3 mRNA are induced by HIV-1 in human oral epithelial cells and exhibit strong anti-HIV-1 activity; in addition, polymorphisms in the DEFB1 gene, which encodes HBD-1, have been associated with resistance/susceptibility to different infections, including HIV-1. Here, we have assessed the association of HBD expression with the ESN phenotype. Peripheral blood and vaginal/endocervical and oral mucosal samples were taken from 47 ESN, 44 seropositive (SP) and 39 healthy controls (HC). HBD-1, 2 and 3 mRNA copy numbers were quantified by real time RT-PCR and A692G/G1654A/A1836G polymorphisms in the DEFB1 gene were detected by restriction fragment length polymorphisms and confirmed by nucleotide sequencing. ESN expressed significantly greater mRNA copy numbers of HBD-2 and 3 in oral mucosa than HC; p=0.0002 and p=0.007, respectively. mRNA copy numbers of HBD-1, 2 and 3 in vaginal/endocervical mucosa from ESN and HC were similar. Homozygosity for the A692G polymorphism was significantly more frequent in ESN (0.39) than in SP (0.05) (p=0.0002). In summary, ESN exhibited enhanced mucosal expression of the innate defense genes HBD-2 and 3; however, additional studies are required to verify these results and the potential association of the A692G polymorphism to the relative resistance of ESN to HIV-1 infection.
AIDS. 2008 Mar 30;22(6):727-35.
HIV-neutralizing immunoglobulin A and HIV-specific proliferation are independently associated with reduced HIV acquisition in Kenyan sex workers.
Hirbod T, Kaul R, Reichard C, Kimani J, Ngugi E, Bwayo JJ, Nagelkerke N, Hasselrot K, Li B, Moses S; Kibera HIV Study Group, MacDonald KS, Broliden K.
Collaborators (16)
Infectious Diseases Unit, Department of Medicine, Solna, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Solna, Sweden.
OBJECTIVES: HIV-neutralizing immunoglobulin A (IgA) and HIV-specific cellular immunity have been described in highly exposed, persistently seronegative (HEPS) individuals, but well controlled studies have not been performed. We performed a prospective, nested case-control study to examine the association of genital IgA and systemic cellular immune responses with subsequent HIV acquisition in high-risk Kenyan female sex workers (FSWs). DESIGN AND METHODS: A randomized trial of monthly antibiotic prophylaxis to prevent sexually transmitted disease/HIV infection was performed from 1998 to 2002 in HIV-uninfected Kenyan FSWs. After the completion of trial, FSWs who had acquired HIV (cases) were matched 1: 4 with persistently uninfected controls based on study arm, duration of HIV-seronegative follow-up, and time of cohort enrolment. Blinded investigators assayed the ability at enrolment of genital IgA to neutralize primary HIV isolates as well as systemic HIV-specific cellular IFNgamma-modified enzyme-linked immunospot and proliferative responses. RESULTS: The study cohort comprised 113 FSWs: 24 cases who acquired HIV and 89 matched controls. Genital HIV-neutralizing IgA was associated with reduced HIV acquisition (P = 0.003), as was HIV-specific proliferation (P = 0.002), and these associations were additive. HIV-specific IFNgamma production did not differ between case and control groups. In multivariable analysis, HIV-neutralizing IgA and HIV-specific proliferation each remained independently associated with lack of HIV acquisition. Genital herpes (HSV2) was associated with increased HIV risk and with reduced detection of HIV-neutralizing IgA. CONCLUSION: Genital HIV-neutralizing IgA and systemic HIV-specific proliferative responses, assayed by blinded investigators, were prospectively associated with HIV nonacquisition. The induction of these immune responses may be an important goal for HIV vaccines.
AIDS. 2008 May 31;22(9):1029-38.
Associations of human leukocyte antigen DRB with resistance or susceptibility to HIV-1 infection in the Pumwani Sex Worker Cohort.
Lacap PA, Huntington JD, Luo M, Nagelkerke NJ, Bielawny T, Kimani J, Wachihi C, Ngugi EN, Plummer FA.
National Microbiology Laboratory, Winnipeg, Canada.
OBJECTIVE: A group of commercial sex workers in the Pumwani Sex Worker Cohort, established in 1985 in Nairobi, Kenya, remain HIV-1 uninfected despite heavy exposure to HIV-1 through active sex work. Previous studies showed that this resistance is associated with a strong CD4+ T-cell response, which suggested that human leukocyte antigen class II antigens are important in resistance/susceptibility to HIV-1 infection. DRB1 is the most polymorphic locus among class II genes and forms haplotypes with DRB3, DRB4 and DRB5. The aim of this study is to investigate the role of DRB alleles/haplotypes on resistance/susceptibility to HIV-1 infection. DESIGN: In total, 1090 women enrolled in the Pumwani cohort were genotyped for DRB1, DRB3, DRB4 and DRB5 using a high-resolution sequence-based method. Allele/haplotype frequencies were compared between HIV-positive women and women who have remained HIV negative for more than 3 years despite frequent exposure. METHODS: Human leukocyte antigen DRB genes were amplified, sequenced and genotyped using a two-step sequence-based method. Allele/haplotype frequencies were determined using PyPop32-0.6.0. Statistical analysis was conducted using SPSS 11.0 for Windows. RESULTS: Three DRB1 alleles were associated with resistance: DRB1*010101 (P = 0.016; odd ratio (OR): 2.55; 95% confidence interval (CI): 1.16-5.61), DRB1*010201 (P = 0.019; OR: 1.86; 95% CI: 1.10-3.15), and DRB1*1102 (P = 0.025; OR: 1.72; 95% CI: 1.07-2.78). DRB1*030201 (P = 0.038; OR: 0.48; 95% CI: 0.23-0.98), DRB1*070101 (P = 0.035; OR: 0.54; 95% CI: 0.30-0.97), DRB1*1503 (P = 0.0004; OR: 0.34; 95% CI: 0.19-0.64), and DRB5*010101 (P = 0.001; OR: 0.37; 95% CI: 0.20-0.67) were associated with susceptibility. The haplotype DRB1*1102-DRB3*020201 was associated with HIV-1 resistance (P = 0.041; OR: 1.68; 95% CI: 1.02-2.78), whereas the haplotypes DRB1*070101-DRB4*01010101 (P = 0.041; OR: 0.52; 95% CI: 0.28-0.98) and DRB1*1503-DRB5*01010101 (P = 0.0002; OR: 0.30; 95% CI: 0.15-0.58) were associated with susceptibility. These associations with resistance/susceptibility to HIV-1 were independent of previously reported alleles HLA-DRB1*01 and HLA-A*2301. CONCLUSION: Our findings indicate that human leukocyte antigen DRB-specific CD4+ T-cell responses are an important factor in resistance/susceptibility to HIV-1 infection.
Curr HIV/AIDS Rep. 2006 Feb;3(1):26-31
Understanding the "lucky few": the conundrum of HIV-exposed, seronegative individuals.
Shacklett BL.
Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, 1 Shields Avenue, Davis, CA 95616, USA.
It has been known for many years that not all individuals who are repeatedly exposed to HIV-1 show evidence of viral replication, seroconvert, and eventually develop disease. Quite apart from those who seroconvert but progress slowly to AIDS (ie, slow progressors, long-term nonprogressors, elite controllers), these rare, exposed seronegatives either resist infection or harbor extremely low levels of virus that may be detected only using ultrasensitive methods (occult infection). The correlates of protection that confer this unique status to a tiny minority of HIV-exposed individuals remain a subject of intense interest, investigation, and controversy, as no single genetic or immunologic parameter has yet been able to fully explain this phenomenon. However, there is general consensus that studying these individuals may provide invaluable information to aid in the design of vaccines and therapeutic approaches. This review describes the major findings on this important topic, with a focus on immunologic studies.
Chin Med J (Engl). 2006 Oct 5;119(19):1616-21
Identification of HIV-1 specific T lymphocyte responses in highly exposed persistently seronegative Chinese.
Liu HW, Hong KX, Ma J, Yuan L, Liu S, Chen JP, Zhang YZ, Ruan YH, Xu JQ, Shao YM.
Division of Virology and Immunology, National Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing 100050, China.
BACKGROUND: Studies of highly exposed persistently seronegative (HEPS) individuals may provide valuable information on mechanisms of protection and on vaccine design. Cellular immune responses play a critical role in containing human immunodeficiency virus. However, the cellular immune responses in HEPS individuals have not been thoroughly assessed at the entire viral genome level. METHODS: Ten HEPS Chinese with a history of frequent penetrative vaginal intercourse (mean frequency, at least once a week), with some unprotected sexual contact occurring in the weeks or days immediately before enrollment, 25 HIV-1 seropositive individuals, 10 HIV-1-seronegative healthy individuals with low-risk sexual behavior and no history suggestive of exposure to HIV-1 infection were enrolled. HIV-1-specific T cell responses were comprehensively analyzed by an interferon-gamma Elispot assay against 770 overlapping peptides spanning all HIV-1 proteins. RESULTS: HIV-1-specific T-cell responses of interferon-gamma secretion were identified in 3 (30%) out of 10 HEPS individuals; the specific cytotoxic T lymphocytes were targeted at Pol (2/10), Env (2/10), and Tat (1/10). HIV-1-specific T-cell responses of interferon-gamma secretion were identified in 20 (80%) out of 25 seropositive intravenous drug users (IDUs), revealing that all HIV-1 proteins and protein subunits could serve as targets for HIV-1-specific CD8(+) T cell responses with 85% recognizing Gag, 80% recognizing Nef, 75% recognizing Pol, 60% recognizing Env, 55% recognizing Vpu, 45% recognizing Vpr, 20% recognizing Vif, 20% recognizing Tat and 15% recognizing Rev in these seropositive individuals. None of the seronegative healthy individuals gave the positive T-cell responses. CONCLUSIONS: About 30% of HEPS Chinese mounted HIV-1 specific T cell immune responses. Cell-mediated immunity against HIV-1 may be developed through non-productive infections.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2006 Oct;28(5):613-7.
[Resistance to HIV-1 infection of CD4 + T lymphocytes in vitro from chinese HIV-1 exposed seronegative individuals]
[Article in Chinese]
Su YL, Shang H, Liu J, Wang SX, Geng WQ, Cui HL, Jiang YJ, Wang YN, Zhang ZN, Wang YT.
Center for AIDS Research, the First Affiliated Hospital, China Medical University, Shenyang 110001, China.
OBJECTIVE: To determine the relative resistance to HIV-1 infection of CD4 + T lymphocytes in HIV-exposed seronegative individuals (ESNs) in China. METHODS: HIV primary isolates were obtained from peripheral whole blood of HIV-infected persons. CD4 + T lymphocytes of Chinese ESNs were separated from peripheral blood mononuclear cells with magnetic cell sorting (MACS). The purified CD4 + T lymphocytes were cocultured with HIV primary isolates. The p24 level was detected and the culture medium was refreshed every 3 days within 2 weeks. RESULTS: For M tropic HIV strains, p24 level was significantly lower in ESN group than in control group (P < 0.05); for some M tropic HIV strains, even no p24 replicated in ESN group. However, T tropic virus strains had no significant difference between these two groups (P > 0.05). CONCLUSION: CD4 + T lymphocytes of Chinese ESNs may possess relative resistance to M tropic HIV strains, which may be one of the main influencing factors that result in ESN.
AIDS. 2006 Sep 11;20(14):1879-83.
CCR5 expression and duration of high risk sexual activity among HIV-seronegative men who have sex with men.
Thomas SM, Tse DB, Ketner DS, Rochford G, Meyer DA, Zade DD, Halkitis PN, Nádas A, Borkowsky W, Marmor M.
Department of Environmental Medicine, New York University School of Medicine, NY 10016-3240, USA
OBJECTIVES: To test the hypothesis that in comparison with those with shorter risk duration, individuals with longer HIV risk duration would have reduced susceptibility to HIV-1 infection as measured by CCR5 expression, and to evaluate whether variation in CCR5 expression could be explained by known genetic polymorphisms. DESIGN AND METHODS: A cross-sectional study of HIV-1 exposed but uninfected men who have sex with men. The risk duration was estimated from self-reported years since first receptive anal intercourse. CCR5 expression on peripheral blood CD4+ monocytes and T cells was determined by flow cytometry. The CCR5-Delta32 mutation and polymorphisms in the CCR5 promoter and CCR2 as well as the copy number of CCL3L1 were analyzed by polymerase chain reaction. Plasma levels of MIP-1alpha (CCL3), MIP-1beta (CCL4) and RANTES (CCL5) were also measured. As risk duration varied with age, analyses were restricted to 67 individuals aged 30-49 years. RESULTS: Multiple linear regression analyses, adjusted for age and race, showed a significant negative association between HIV risk duration and CCR5 expression on monocytes (P = 0.01), and in a separate model, a similar negative association with CCR5 expression on T cells (P = 0.03). Low CCR5 expression was attributable mainly to CCR5-Delta32 heterozygosity and the CCR5-59029G allele. CONCLUSIONS: We confirmed a role for reduced CCR5 expression in HIV-1 resistance. CCR5-Delta32 heterozygosity and the CCR5-59029G allele were significant predictors of low CCR5 expression. Individuals with high CCR5 expression who resisted infection despite long HIV risk duration form an interesting group within which to search for additional mechanisms of resistance to HIV infection.
J Clin Immunol. 2006 Sep;26(5):476-84. Epub 2006 Jul 25.
Gene polymorphisms in CCR5, CCR2, CX3CR1, SDF-1 and RANTES in exposed but uninfected partners of HIV-1 infected individuals in North India.
Suresh P, Wanchu A, Sachdeva RK, Bhatnagar A.
Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
Repeated exposure to human immunodeficiency virus (HIV) does not always result in infection. Understanding the mechanisms that give protection against progressive infection with HIV may help in the development of a vaccine. In order to determine the influence of host genetic factors on HIV resistance, we studied 35 exposed but uninfected (EU) partners of HIV-1 infected individuals for polymorphisms in multiple chemokine and chemokine receptor genes and compared the results with those for 75 HIV-1 seronegative normal healthy controls (HC) and 50 HIV infected controls. There was no association between CCR5-Delta32, CCR2-64I, CX3CR1-280 M, CX3CR1-249I, SDF-3'A, RANTES-28G and RANTES-403A polymorphisms and susceptibility against HIV in our cohort of EU individuals. An increased frequency of SDF-1 3'A and RANTES-403A genotypes was present in EU individuals but the difference was not statistically significant when compared to healthy and HIV infected controls. These observations suggest that mechanisms other than genetic mutations of these genes might be responsible for resistance to HIV infection in these individuals.
J Acquir Immune Defic Syndr. 2006 Aug 1;42(4):412-9.
HIV-specific antibodies but not t-cell responses are associated with protection in seronegative partners of HIV-1-infected individuals in Cambodia.
Nguyen M, Pean P, Lopalco L, Nouhin J, Phoung V, Ly N, Vermisse P, Henin Y, Barré-Sinoussi F, Burastero SE, Reynes JM, Carcelain G, Pancino G.
Institut Pasteur du Cambodge, Phnom Penh, Cambodia.
To study biological factors related to protection against HIV-1 infection in Cambodia, we recruited 48 partners of HIV-1-infected patients who remained uninfected (exposed uninfected individuals, EUs) despite unprotected sexual intercourse for more than 1 year and 49 unexposed controls (UCs). HIV-1-specific antibodies (IgA anti-gp41 and IgG anti-CD4-gp120 complex), T-cell responses, and cellular factors that may be involved in protection (peripheral blood mononuclear cell [PBMC] resistance to HIV-1 infection and beta-chemokine production) were evaluated. Anti-HIV-1 antibodies were higher in EUs than those in UCs (P = 0.01 and P = 0.04 for anti-gp41 and anti-CD4-gp120, respectively). We observed a decreased susceptibility to a primary Cambodian isolate, HIV-1KH019, in EU PBMCs as compared with UC PBMCs (P = 0.03). A weak T-cell response to one pool of HIV-1 Gag peptides was found by ELISpot in 1 of 19 EUs. Whereas T-cell specific immunity was not associated to protection, our results suggest that HIV-specific humoral immunity and reduced cell susceptibility to infection may contribute to protection against HIV-1 infection in Cambodian EUs.
Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2006 Jun;20(2):72-4.
[Epidemiologic study and HLA analysis of highly exposed to HIV but persistently seronegative subjects (HEPS) in commercial blood donors in China]
[Article in Chinese]
Xu KY, Dong T, Lun WH.
Beijing Ditan Hospital, Beijing 100011, China.
BACKGROUND: To investigate epidemiology and HLA typing of highly exposed to HIV but persistently seronegative subjects (HEPS) in commercial blood donors in China. METHODS: This was a cohort study for epidemiologic characteristics of highly exposed but persistently seronegative subjects. PCR with sequence-specific primer and PCR-SSP for HLA typing were applied. RESULTS: Eight HEPS were identified. Compared HLA typing with seropositive couple, high frequency of HLA-a24, HLA-B40 genotyping was observed. CONCLUSION: Highly exposed to HIV but persistently seronegative subjects in commercial blood donors in China had high frequency of HLA-A24 and HLA-B40 genotype.
Virol J. 2006 Jun 29;3:52.
Human Immunodeficiency Virus type 1 in seronegative infants born to HIV-1-infected mothers.
Vázquez Pérez JA, Basualdo Sigales MC, Reyes-Terán G, Gudiño Rosales JC, Soler ClaudÃn C.
Unidad de Servicios Para Diagnóstico y Referencia en VIH, Instituto de Investigaciones Biomédicas UNAM/SecretarÃa de Salud del DF, México D.F.
BACKGROUND: Some individuals repeatedly exposed to Human Immunodeficiency Virus do not seroconvert and are resistant to HIV infection. Here, in a pediatric cohort of HIV seronegative infants born of HIV-infected mothers, we have studied eight non-breastfed children in whom viral DNA was detected in their PBMC. Our objective was to assess whether silent infection in these children can be explained by the presence of integrated viral DNA. METHODS: The presence of viral DNA was corroborated by nested PCR with primers for gag and the nef/LTR regions of HIV-1. Integration of HIV DNA into the host genome was assessed by an Alu-LTR PCR. Amplicons were sequenced and phylogenetic analyzes were done. RESULTS: HIV-1 DNA was detected in the earliest available PBMC sample from all eight infants, and two of them tested positive for HIV DNA at 2 years of age. Nested PCR resulted in the amplification of gag, nef/LTR and Alu-LTR fragments, which demostrated that HIV-1 DNA was integrated in the host cell genome. Each individual has a characteristic sequence pattern and is different from the LTR sequence of HXB2 prototype virus and other Mexican isolates. CONCLUSION: HIV-1 DNA was observed in PBMC from HIV exposed seronegative children in this pediatric cohort.
J Immunol. 2005 Nov 1;175(9):6117-22.
Low-level CD4+ T cell activation is associated with low susceptibility to HIV-1 infection.
Koning FA, Otto SA, Hazenberg MD, Dekker L, Prins M, Miedema F, Schuitemaker H.
Department of Clinical Viro-immunology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
Different features have been associated with low susceptibility to HIV type 1 (HIV-1) infection in exposed seronegative individuals. These include genetic make-up such as homozygosity for the CCR5-Delta32 allele and the presence of HIV-specific CTLs. We studied immune activation and immune responsiveness in relation to HIV-1 susceptibility in 42 high-risk seronegative (HRSN) participants of the Amsterdam Cohort Studies and 54 men from the same cohort who were seronegative at the moment of analysis but later became HIV seropositive. HRSN had higher naive (CD45RO CD27) CD4 and CD8 T cell numbers and lower percentages of activated (HLADR CD38, CD70) CD4 and proliferating (Ki67) CD4 and CD8 T cells, irrespective of previous episodes of sexually transmittable infections. Furthermore, whole blood cultures from HRSN showed lower lymphoproliferative responses than healthy laboratory controls. These data suggest that low levels of immune activation and low T cell responsiveness may contribute to low HIV susceptibility.
J Virol. 2005 Sep;79(18):11677-84.
Combined effect of CCR5-Delta32 heterozygosity and the CCR5 promoter polymorphism -2459 A/G on CCR5 expression and resistance to human immunodeficiency virus type 1 transmission.
Hladik F, Liu H, Speelmon E, Livingston-Rosanoff D, Wilson S, Sakchalathorn P, Hwangbo Y, Greene B, Zhu T, McElrath MJ.
Fred Hutchinson Cancer Research Center, Clinical Research Division, Program in Infectious Diseases, 1100 Fairview Ave. N., P.O. Box 19024, D3-100, Seattle, WA 98109-1024, USA.
Exposed seronegative individuals (ES) with persistent high-risk sexual behavior may be less susceptible to human immunodeficiency virus type 1 (HIV-1) infection because they carry the chemokine receptor (CR) gene alleles CCR5 open reading frame (ORF) Delta32, CCR5 promoter -2459G, or CCR2 ORF 64I (CCR2-64I), all of which have been found to diminish HIV-1 infectivity and/or disease progression. To investigate this, we determined the haplotypes for these three genetic loci in 93 ES and 247 low-risk control individuals. To test if protective haplotypes exert their effect by modulating CR expression, we measured the protein expression of CCR5 and CXCR4 on circulating CD4+ T cells and CD14+ monocytes in 71 ES and 92 controls. To avoid investigator bias, the analysis was performed without knowledge of each subject's risk and genotype. The CCR5 -2459G allele was significantly enriched in ES Caucasian men, who constituted the majority (84%) of the ES cohort, compared to the control Caucasian men (P = 0.02). This increase was mostly attributable to a higher frequency of the -2459 A/G versus the -2459 A/A genotype in individuals heterozygous for the delta32 allele (P = 0.012). No protective influence of the CCR2-64I allele was observed. The haplotypes CCR5 ORF delta32/CCR5 -2459A (in complete linkage disequilibrium) and CCR5 ORF wt/CCR5 -2459G had a cumulative negative effect on the expression of CCR5, since we measured significantly reduced CCR5 densities on both T-helper cells and monocytes only when both haplotypes were present. Densities of CCR5 on lymphocytes and monocytes were correlated (r = 0.59; P < 0.0001), indicating concordance of CCR5 expression patterns across different cell types. We conclude that the CCR5 ORF delta32/wt-CCR5 -2459 A/G genotype combination offers an advantage in resisting sexual HIV-1 transmission and that this effect is mediated by a relative paucity of CCR5 on potential target cells of HIV-1.
Virol J. 2005 Aug 17;2:65.
Evidence of HIV exposure and transient seroreactivity in archived HIV-negative severe hemophiliac sera.
Tenenbaum SA, Morris CA, Alexander SS, McFerrin HE, Garry RF, Leissinger CA.
Department of Biomedical Sciences, Ge*NY*Sis Center for Excellence in Cancer Genomics, University at Albany-SUNY, Albany, NY, USA.
BACKGROUND: Approximately 25% of hemophiliacs that were frequently exposed to blood clotting factor concentrates (CFCs) contaminated with human immunodeficiency virus (HIV) are presently HIV seronegative. In this study, we sought to determine if some of these individuals were at any time transiently HIV seropositive. In the early to mid-1980s the majority of severe hemophilia patients were exposed to CFCs contaminated with HIV. Although many of these hemophiliacs became HIV-positive, a small percentage did not become infected. To determine if some of these individuals successfully resisted viral infection, we attempted to document the presence of transient HIV reactive antibodies in archived plasma samples (1980-1992) from currently HIV-negative severe hemophiliacs who had a high probability of repeated exposure to HIV contaminated CFC. Archived plasma samples were retrospectively tested using an FDA approved HIV-1Ab HIV-1/HIV-2 (rDNA) enzyme immunoassay (EIA) and a HIV-1 Western blot assay (Wb), neither of which were commercially available until the late 1980s, which was after many of these samples had been drawn. RESULTS: We found that during the high risk years of exposure to HIV contaminated CFC (1980-1987), low levels of plasma antibodies reactive with HIV proteins were detectable in 87% (13/15) of the haemophiliacs tested. None of these individuals are presently positive for HIV proviral DNA as assessed by polymerase chain reaction (PCR). CONCLUSION: Our data suggest that some severe hemophiliacs with heavy exposure to infectious HIV contaminated CFC had only transient low-level humoral immune responses reactive with HIV antigens yet remained HIV-negative and apparently uninfected. Our data supports the possibility of HIV exposure without sustained infection and the existence of HIV-natural resistance in some individuals.
J Virol. 2005 May;79(10):6551-3.
Low levels of human immunodeficiency virus type 1 DNA in high-risk seronegative men.
Koning FA, van der Vorst TJ, Schuitemaker H.
Sanquin Research at CLB, Dept. of Clinical Viro Immunology, Plesmanlaan 125, 1066 CX Amsterdam, The Netherlands.
We detected human immunodeficiency virus type 1 (HIV-1) DNA at very low levels in sequential peripheral blood mononuclear cell samples of five out of six high-risk, seronegative, homosexual men and five out of five individuals 7.8 to 1.6 years prior to seroconversion. These data indicate a high prevalence of low-level HIV-1 DNA in exposed seronegative individuals.
AIDS. 2005 Apr 29;19(7):653-61.
Distinct patterns of HIV-specific memory T lymphocytes in HIV-exposed uninfected individuals and in HIV-infected patients.
Schenal M, Lo Caputo S, Fasano F, Vichi F, Saresella M, Pierotti P, Villa ML, Mazzotta F, Trabattoni D, Clerici M.
Immunology DISP LITA Vialba, University of Milano, Milano, Italy.
BACKGROUND: Repeated exposure to HIV is not always associated with infection and multiple cohorts of HIV-exposed but seronegative individuals (ESN) have been described. HIV-specific CD4 and CD8 T lymphocytes are detected both in HIV patients and in ESN; we verified whether different patterns of HIV-specific memory T lymphocytes would be detected in individuals in whom exposure to HIV results or does not result in infection. METHODS: Gag-specific T cells were analysed in 15 ESN, 14 HIV patients, and 15 healthy controls using extensive flow cytometry analysis. RESULTS: Data confirmed that gag-specific T lymphocytes are present in ESN. Gag-specific T cells mainly secrete interleukin-2 in ESN and interferon-gamma in HIV patients. In addition the CD4/CD8 and the memory/naive ratios are altered, central memory (45RA-/CCR7+) CD4 and CD8 T lymphocytes are more abundant, and terminally differentiated (45RA+/CCR7- and 27-/28-) CD8 T lymphocytes are augmented in ESN individuals. CONCLUSIONS: Exposure to HIV occurs in high risk seronegative individuals; the observation that naive cells and CM are skewed in ESN indicate that this exposure is robust enough to modulate the CM/EM ratio. The increase in late effectors and in natural killer cells seen in ESN suggests a role for these cells in preventing actual infection.
J Infect Dis. 2005 Jan 1;191(1):20-4. Epub 2004 Dec 1.
CD4+ T cell responses in HIV-exposed seronegative women are qualitatively distinct from those in HIV-infected women.
Alimonti JB, Koesters SA, Kimani J, Matu L, Wachihi C, Plummer FA, Fowke KR.
Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, Manitoba R3E 0W3, Canada.
The immune response of human immunodeficiency virus (HIV)-exposed seronegative (ESN) women may be qualitatively different from that in those infected with HIV (HIV(+)). In a cohort of female commercial sex workers in Nairobi, Kenya, we found significantly lower (P< or =.01) levels of CD4(+)-specific immune activation and apoptosis in the ESN women compared with those in the HIV(+) women. Compared with the HIV(+) women, a lower proportion of the ESN women showed p24 peptide pool responses by the short-term, CD4(+)-specific, interferon (IFN)- gamma intracellular cytokine staining assay, whereas the proportion showing responses by the long-term, CD8(+)-depleted T cell proliferation assay was similar. Interestingly, the ESN responders had a 4.5-fold stronger proliferation response (P=.002) than the HIV(+) group. These data suggest that, compared with those in HIV(+) women, CD4(+) T cells in ESN women have a much greater ability to proliferate in response to p24 peptides.
Immunol Res. 2004;29(1-3):161-74.
Insights into the role of host genetic and T-cell factors in resistance to HIV transmission from studies of highly HIV-exposed Thais.
McNicholl JM, Promadej N.
Immunogenetics Section, HIV Immunology and Diagnostics Branch, National Center for HIV, STD and TB Prevention, Centers for Disease Control and Prevention, 1600 Clifton Road NE, Atlanta, GA 30333, USA.
Studies of resistance to HIV-1 transmission are likely to be valuable for the design of vaccines and other efforts to prevent HIV. Here, we review the T-cell and genetic factors associated with resistance to HIV-1 transmission in studies of highly exposed but persistently seronegative (HEPS) women from northern Thailand. Women were enrolled in two sex-worker studies and in a discordant couple study. We performed Cr51 cytotoxic T lymphocyte (CTL), interferon-gamma (IFN-gamma) ELISPOT, and proliferation assays as well as genetic studies, including HLA-class I typing. CTL and ELISPOT studies showed a skewing of T-cell responses to conserved HIV-1 proteins in HEPS, but not in HIV-1-seropositive women. T-cell responses were extremely long-lived in some HEPS women. In the two sex-worker studies, HLA-A11 was associated with resistance to HIV-1 transmission. These data provide promise for the ability of CTL to control HIV and emphasize the importance of developing HIV vaccines that stimulate strong, long-lasting Tcell responses.
AIDS. 2004 May 21;18(8):1117-26.
Correlates of resistance to HIV-1 infection in homosexual men with high-risk sexual behaviour.
Koning FA, Jansen CA, Dekker J, Kaslow RA, Dukers N, van Baarle D, Prins M, Schuitemaker H.
Department of Clinical Viro Immunology, Sanquin Research at CLB and Landsteiner
Laboratory of the Academic Medical Centre, University of Amsterdam, The Netherlands.
OBJECTIVE: To investigate possible correlates of HIV resistance in participants from the Amsterdam Cohort of Homosexual men who have remained HIV seronegative despite high-risk sexual behaviour. DESIGN/METHODS: We studied in vitro HIV-1 susceptibility and adaptive and innate immunity in 29 high-risk seronegative (HRSN) and 15 HIV-negative pre-seroconversion (pre-SC) homosexual men from the same Amsterdam Cohort Study (ACS) who seroconverted to HIV-1 positive during active follow-up. Host genetics were compared between HRSN and HIV-positive ACS participants. RESULTS: We found lower in vitro susceptibility for a CCR5-using (R5) HIV-1 variant, higher RANTES production levels, but no difference in coreceptor expression in HRSN as compared with pre-SC controls. Reduced R5 in vitro susceptibility of two HRSN tested was restored to normal levels by addition of antibodies against beta-chemokines. A higher proportion of HRSN carried the SDF-1 3'A variant and HLA-A*11, A*31 and Cw*15 alleles. ELIspot analysis with HIV-1 peptide stimulation revealed low frequencies of HIV-1-specific CD8 interferon-gamma producing cytotoxic T cells in both HRSN and pre-SC controls. CONCLUSIONS: Low in vitro R5 susceptibility of cells from the HRSN men was due to beta-chemokine mediated inhibition of virus replication. The presence of HIV-1 specific cytotoxic T cells in both HRSN and pre-SC participants may signify exposure to the virus rather than protection from infection. Host genetic characteristics and other factors affecting innate immunity may contribute to differential resistance to HIV-1 infection among exposed seronegative individuals.
J Infect Dis. 2004 May 1;189(9):1705-13. Epub 2004 Apr 19.
Distinct patterns of peripheral HIV-1-specific interferon- gamma responses in exposed HIV-1-seronegative individuals.
Kebba A, Kaleebu P, Rowland S, Ingram R, Whitworth J, Imami N, Gotch F.
Department of Immunology, Imperial College, London, Chelsea and Westminster Hospital, London, United Kingdom.
It is unclear how human immunodeficiency virus (HIV) type 1-specific immune responses in exposed seronegative (ESN) individuals differ from those in HIV-1-infected subjects. By use of overlapping peptides spanning Gag, Tat, Nef, Vif, Vpr, and Vpu, peripheral blood mononuclear cells from ESN individuals, their seropositive (SP) partners, and unexposed seronegative control subjects were screened for interferon- gamma production. Responses were more frequent (95.7% vs. 20%), of a higher magnitude (9-fold), and of wider breadth (median number of peptides recognized, 18 vs. 2.5) in SP than in ESN individuals. Peptides recognized by ESN individuals were less frequently recognized by their SP partners. SP subjects infrequently recognized peptides from Vif, and such responses were subdominant; among ESN individuals, this HIV-1 protein was most frequently recognized. Immunodominant peptides recognized by SP subjects tended to be from relatively conserved regions, whereas peptides recognized by ESN individuals were associated with slow disease progression.
AIDS Res Hum Retroviruses. 2004 Jan;20(1):67-75.
HIV type 1 antigen-responsive CD4+ T-lymphocytes in exposed yet HIV Type 1 seronegative Ugandans.
Kebba A, Kaleebu P, Serwanga J, Rowland S, Yirrell D, Downing R, Gilmour J, Imami N, Gotch F, Whitworth J.
Medical Research Council's Programme on AIDS in Uganda, UVRI, Entebbe, Uganda.
CD4(+) T cell help is important for the functionality of CD8(+) cytotoxic T-lymphocytes (CTLs) in limiting viral replication and may contribute to mediation of apparent resistance to HIV-1 infection in exposed seronegative (ESN) individuals. Using five HIV-1 antigens in an intracellular cytokine assay, the presence of specific antigen-responsive interferon- gamma-positive (IFN-gamma(+)) CD69(+) CD4(+) T-lymphocytes was evaluated in ESNs, their seropositive partners, and unexposed seronegative controls. Ten ESNs (five females, five uncircumcised males) were identified from 10 HIV-1 serodiscordant couples with a history of frequent unprotected sexual intercourse. All ESNs and controls were negative on two EIAs and for HIV-1 proviral DNA. The frequency of ESNs with antigen-responsive IFN-gamma(+) CD69(+) CD4(+) T-lymphocytes ranged from three to five of eight for the different HIV-1 antigens. Six of eight ESNs tested had a positive response to at least one of the five antigens. Responses were on average 3.5 times higher among seropositives compared to ESNs and absent in the five unexposed controls. A negative correlation was noted between responses in ESNs and the plasma viral load of their seropositive spouse. Clade-specific and cross-clade reactivity were noted in both ESNs and seropositive partners tested. The findings confirm that ESNs are in a state of HIV-1-specific immune activation and suggest that HIV-1-specific IFN-gamma(+) CD69(+) CD4(+) T-lymphocytes in addition to HIV-1-specific CD8(+) CTLs already described by others are potential immunological correlates of protection from persistent HIV-1 infection.
J Infect Dis. 2004 Feb 15;189(4):602-10. Epub 2004 Jan 29.
HIV-specific T helper responses and frequency of exposure among HIV-exposed seronegative female sex workers in Abidjan, Cote d'Ivoire.
Jennes W, Vuylsteke B, Borget MY, Traore-Ettiegne V, Maurice C, Nolan M, Nkengasong JN, Kestens L.
Department of Microbiology, Laboratory of Immunology, Institute of Tropical Medicine, Nationalestraat 155, 2000 Antwerp, Belgium.
BACKGROUND: The characteristics of human immunodeficiency virus (HIV) exposure that determine the induction of HIV-specific T cells and, in particular, T helper cells are not well understood. METHODS: HIV-1 Gag- and Env-specific T helper cells were analyzed by use of an interferon (IFN)- gamma enzyme-linked immunosorbent spot (ELISPOT) assay and by use of IFN- gamma secretion flow cytometry. Responses among HIV-exposed seronegative (ESN) female sex workers (FSWs) were compared with responses among HIV-seropositive FSWs and HIV-seronegative female blood donors from Abidjan, Cote d'Ivoire. RESULTS: Low-level ELISPOT responses were detected in 8 (20%) of 40 ESN FSWs. All of 25 HIV-seropositive FSWs had high-level ELISPOT responses. HIV-specific CD4+ T cells and, occasionally, CD8+ T cells were detected by secretion flow cytometry in 3 (38%) of 8 ESN FSWs and in 4 (80%) of 5 HIV-seropositive FSWs. ESN FSWs with detectable HIV-specific T helper responses had more clients on the previous working day (P=.02) and more exposures to HIV per month (P=.02) and tended to have a lower total duration of commercial sex work. CONCLUSIONS: These findings demonstrate that the presence of HIV-specific T helper cells in ESN FSWs is associated with the frequency, rather than the duration, of exposure to HIV. The data may have important implications for the evaluation of HIV vaccine efficacy.
AIDS. 2003 Nov 7;17(16):2299-311.
Evidence for Gag p24-specific CD4 T cells with reduced susceptibility to R5 HIV-1 infection in a UK cohort of HIV-exposed-seronegative subjects.
Eyeson J, King D, Boaz MJ, Sefia E, Tomkins S, Waters A, Easterbrook PJ, Vyakarnam A.
Department of Immunology, Guy's, King's and St Thomas' School of Medicine and Dentistry, King's College Hospital, London SE5 9NU, UK.
AIM: To characterize HIV-1 Gag p24-specific CD4 cell responses in HIV-exposed-seronegative (ES) individuals. METHODOLOGY: Twelve ES individuals, of diverse ethnicity and wild type for the CCR5 Delta-32 mutation, were identified. Controls were HIV-negative blood donors. Gag p24-specific and total Vbeta+ CD4 cells that expressed MIP-1beta, IFN-gamma and IL-2 were enumerated by intracytoplasmic cytokine staining. beta-Chemokine expression was correlated with susceptibility to R5 HIV-1 infection, as measured by polymerase chain reaction for integrated HIV-1 and by p24 enzyme-linked immunosorbent assay. RESULTS: Similar numbers of mitogen-stimulated and Vbeta+ MIP-1beta+, IFN-gamma+ and IL-2+ T cells were found in ES and HIV-negative control subjects. However, all ES subjects tested had an HIV Gag p24-specific MIP-1beta+, IFN-gamma+ and IL-2+ CD4 T-cell response that was rare in controls. p24-Specific cells of all ES but no control subjects could be expanded by in-vitro Ag/IL-2 stimulation, and when re-stimulated with an overlapping peptide series showed evidence of a broad CD4 cell memory response directed against multiple regions of Gag p24. Mitogen-stimulated ES CD4 cells were as susceptible to HIV infection as those from control subjects, but p24-specific IFN-gamma+ CD4 cells of six out of seven ES subjects tested were less susceptible to R5 HIV-1 infection than the counterpart fraction depleted of p24-specific IFN-gamma+ cells. The addition of blocking anti-beta-chemokine antibodies did not promote R5 HIV-1 infection of p24-specific IFN-gamma+ cells. CONCLUSION: Specific CD4 cell immunity, characterized by a broadly directed memory Gag-p24 CD4 cell response and reduced susceptibility of specific CD4 cells to R5 HIV-1 infection, is a likely correlate of non-transmission.
AIDS Res Hum Retroviruses. 2003 Aug;19(8):661-5.
Polymorphisms in the CCR5 coding and noncoding regions among HIV type 1-exposed, persistently seronegative female sex-workers from Thailand.
Yang C, Li M, Limpakarnjanarat K, Young NL, Hodge T, Butera ST, McNicholl JM, Mastro TD, Lal RB.
HIV Immunology and Diagnostics Branch, Division of AIDS, STD, and TB Laboratory Research, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, GA 30333, USA.
Resistance to HIV-1 infection despite repeated exposures has been associated with one or more HIV-specific responses, enhanced nonspecific immune modifications, and/or host genetic polymorphisms in certain individuals (highly exposed, persistently seronegative, HEPS). In the present investigation, we focused on the CCR5 gene polymorphisms and the association of such mutations to resistance to HIV-1 infection among 12 HEPS women in Chiang Rai, northern Thailand, and compared our findings with data from 10 HIV-1-infected and 9 HIV-1-uninfected unexposed women from the same geographic area. Although we have previously shown that none of the Thai women carried the Delta32 mutation, further analysis of the CCR5 coding gene region revealed that none of the women had other mutations that affect coreceptor activity (C101X or FS299) or chemokine responses (C20S, A29S, L55Q, C178R). Analysis of the CCR5 promoter region revealed that the CCR5 haplogroup C (HHC; 60%) was the predominant haplogroup among these women. Comparative analysis of the frequencies of different haplogroups among the three groups did not reveal any statistically significant differences (p 0.05). However, we did find that two individuals from the HEPS group were homozygous for HHF*2 (the CCR2b- 64I bearing haplogroup) compared to none from the HIV-1-infected and -uninfected groups. There was no detectable difference in specific CCR5 haplogroups and their ability to mediate env fusion or to mediate HIV-1 infection in vitro. These data suggest that homozygosity of the HHF*2 haplogroup may be one of the factors that mediate resistance to HIV-1 infection in this cohort of HEPS women.
AIDS Rev. 2003 Apr-Jun;5(2):87-103.
Resistance to HIV-1 infection: lessons learned from studies of highly exposed persistently seronegative (HEPS) individuals.
Kulkarni PS, Butera ST, Duerr AC.
HIV and Retrovirology Branch, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, NE, Atlanta, GA 30333, USA.
The medical, social, and economic impact of the human immunodeficiency virus (HIV) epidemic has underscored the need to quickly develop effective control strategies. Vigorous efforts to develop a vaccine and therapeutic agents have not yet succeeded in containing the spread of the virus. Studies of persons who remain uninfected despite extensive exposure to HIV continue to provide valuable information on mechanisms of natural protection, which can then be applied to vaccine design. Natural resistance to infection has been studied in multiple high-risk cohorts, with resistance attributed to a combination of innate, genetic, and acquired immune system-mediated mechanisms. The relative contributions of these factors to natural resistance to HIV-1 infection and possible ways in which they can be applied to vaccine design are discussed.
J Virol. 2003 Jun;77(11):6108-16.
Persistence of extraordinarily low levels of genetically homogeneous human immunodeficiency virus type 1 in exposed seronegative individuals.
Zhu T, Corey L, Hwangbo Y, Lee JM, Learn GH, Mullins JI, McElrath MJ.
Department of Laboratory Medicine, University of Washington School of Medicine, Seattle 98195, USA.
Some individuals remain inexplicably seronegative and lack evidence for human immunodeficiency virus type 1 (HIV-1) infection by conventional serologic or virologic testing despite repeated high-risk virus exposures. Here, we examined 10 exposed seronegative (ES) individuals exhibiting HIV-1-specific cytotoxicity for the presence of HIV-1. We discovered HIV-1 DNA in resting CD4(+) T cells (mean, 0.05 +/- 0.01 copies per million cells) at multiple visits spanning 69 to 130 weeks in two ES individuals at levels that were on average 10(4)- to 10(6)-fold lower than those of other HIV-1-infected populations reported. Sequences of HIV-1 envelope and gag genes remained markedly homogeneous, indicating little to undetectable virus replication. These results provide the evidence for HIV-1 infection in ES individuals below the detection limit of standard assays, suggesting that extraordinary control of infection can occur. The two HIV-infected ES individuals remained healthy and were not superinfected with other HIV-1 strains despite continued high-risk sexual exposures to multiple HIV-infected partners. Understanding the mechanisms that confer diminished replicative capacity of HIV-1 in these hosts is paramount to developing strategies for protection against and control of HIV-1 infection.
Unfortunately, Cooler's Modus operandi is to either repeat denialist quotes without verifying that they are true or simply pulling new ones out of his ass without doing any research...often times both.
S:
Is it possible for the co. to make me a loan?
You guys can add the Padian study to this list where there was no seroconversions in thousands of instances of serodiscordant couples having all kinds of sex.
These studies are pretty useless, simply because the assume a priori that HIV is highly contagious, and when they find out it is not, (which is pretty obvious since the Lovers of Magic, ,Eazy e etc have all tested negative) they come up with all types of genetic ad hoc excuses. They never test the most obvious hypothesis, that HIV is barely contagious at all, which all the data implies.
Chris you have not even investigated the JFK, 9/11 theories, hell you have not even probably read what the debunkers opinion are. My point in that post about Vietnam and Iraq is precedent, if you don't have any rebuttals to what I said about the the United States intentionally murdering millions of people based on propaganda and deception, you are pretty crazy to dismiss the simple notion that the Warren Commision etc. might not be revealing the whole truth, and if this Government and CIA would kill millions abroad and at home with fraudulent wars, coups, supporting both sides of the Iran-Iraq war, It doesn't sound too unlikely that these crooks would pull off some messed up stuff at home. To rational person this would make sense. Since you have never investigated any of these theories at all, you are in no position to have any opinion on 9/11 or JFK etc.
So you are just playing a game of guilt by association, you can not debate anything in terms of evidence, so you must label me as "crazy." These type of tactics would get you laughed out of any courtroom.
Defendent x position is crazy.
Judge. Explain overwhelming evidence that your theory is correct and the defendents is not, especially since there is ample precedent for the defendents accusation of the government carrying out horrific crimes in the past.
I can not provide any evidence for my theories or rebut the defendents, he is just crazy!
Verdict: Not guilty. Chris you'd make a horrible lawyer.
Coolaid,
You are the one making claims, the burden of proof rests with you.
No you are the one making claims, that Lee Harvey Oswald acted alone, and that 19 hijackers were present at the airports. Also you are saying that there is nothing worth investigating in any alternative theories.
14 of the hijackers never have appeared on the airports cams, the 5 that were, were released 3 years later. Please provide the overwhelming evidence that 19 hijackers were at the airports( All the CCTV pictures, and sworn witness statements, ticket stubs etc.) If a 7-11 was robbed you'd have all this evidence within days.
Also provide the overwhelming evidence Lee Harvey Oswald acted alone, and why if the shot came from behind, why did JFK's head go back and to the left, when most forensic experts like Dr. Cyril Wecht say that obviously implies the shot came from the front. Waiting.
I'm not holding my breath since none of you clowns have been able to cite and describe the imoportence of the papers that proved HIV was a fatal disease justified AZT being administered for life in 1987, the IOM recommending billions in research in 1985 for HIV and the DHHS saying the probable cause of AIDS has been found and a vaccine would be developed in 1984.
Importance
OK, here are some transmission studies then. As the average prospective follow up of couples in the Padian study was only a year or so, you'll find many larger studies here with much longer follow up. I think denialists get confused as to what science is, because the people who promote denial approach it by deciding their view and then cherry-picking, manipulating and misrepresenting data to fit whatever that view is. I propose that this approach be given a new name: denience (TM).
If you think the human leukocyte antigen system is an ad hoc excuse cooler I hope you never need to get a transplant.
J Immunol. 2008 Aug 15;181(4):2626-35.
Human leukocyte antigen class I genotypes in relation to heterosexual HIV type 1 transmission within discordant couples.
Tang J, Shao W, Yoo YJ, Brill I, Mulenga J, Allen S, Hunter E, Kaslow RA.
Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Differences in immune control of HIV-1 infection are often attributable to the highly variable HLA class I molecules that present viral epitopes to CTL. In our immunogenetic analyses of 429 HIV-1 discordant Zambian couples (infected index partners paired with cohabiting seronegative partners), several HLA class I variants in index partners were associated with contrasting rates and incidence of HIV-1 transmission within a 12-year study period. In particular, A*3601 on the A*36-Cw*04-B*53 haplotype was the most unfavorable marker of HIV-1 transmission by index partners, while Cw*1801 (primarily on the A*30-Cw*18-B*57 haplotype) was the most favorable, irrespective of the direction of transmission (male to female or female to male) and other commonly recognized cofactors of infection, including age and GUI. The same HLA markers were further associated with contrasting viral load levels in index partners, but they had no clear impact on HIV-1 acquisition by the seronegative partners. Thus, HLA class I gene products not only mediate HIV-1 pathogenesis and evolution but also influence heterosexual HIV-1 transmission.
AIDS. 2008 Aug 20;22(13):1667-71.
Herpes simplex virus 2 serostatus and viral loads of HIV-1 in blood and semen as risk factors for HIV transmission among men who have sex with men.
Butler DM, Smith DM, Cachay ER, Hightower GK, Nugent CT, Richman DD, Little SJ.
University of California, San Diego, California, USA.
OBJECTIVE: Human immunodeficiency virus type 1 blood plasma viral load is correlated with the sexual transmission of HIV, although transmission from men involves virus from semen instead of blood. We quantified HIV-1 RNA in the blood and semen of men who did or did not transmit HIV to their sex partners. We compared the relationships of HIV-1 transmission risk with blood plasma viral load, seminal plasma viral load, herpes simplex virus 2 serostatus and other factors. DESIGN: A case-control study. METHODS: Participants were men evaluated for primary HIV infection and their recent male sex partners. They were interviewed, and clinical specimens were collected. Epidemiologic and phylogenetic linkages were determined by history and molecular techniques. Couples were grouped on the basis of transmission after exposure. Fisher's exact test and Wilcoxon tests were used for comparisons between groups. Multivariable logistic regressions were fit to identify independent predictors of transmission. RESULTS: HIV-transmitting partners (n = 15) had a higher median seminal plasma viral load (P < 0.015) and median blood plasma viral load (P < 0.001) than nontransmitting partners (n = 32). Herpes simplex virus 2 serostatus was associated with transmission only when the HIV-infected source partner was herpes simplex virus 2 seropositive and the HIV-exposed partner was not (odds ratio 16, P < 0.03). Adjusting for other factors, HIV transmission was significantly associated with blood plasma viral load (odds ratio 13.4, P < 0.02) but not seminal plasma viral load (odds ratio 0.69, P = not significant). CONCLUSION: Blood and seminal plasma viral load were both associated with human immunodeficiency virus type 1 transmission, but blood plasma viral load was the stronger predictor in this cohort. Herpes simplex virus 2 coinfection was associated with the risk of transmission but not acquisition of human immunodeficiency virus type 1.
Sex Transm Dis. 2008 Nov;35(11):912-5.
Sexual transmission of HIV-1 among serodiscordant couples in Porto Alegre, southern Brazil.
Melo MG, Santos BR, De Cassia Lira R, Varella IS, Turella ML, Rocha TM, Nielsen-Saines K.
Department of Infectious Diseases, Hospital Nossa Senhora da Conceição/GHC, Porto Alegre, Brazil.
BACKGROUND: A cohort of 93 heterosexual HIV serodiscordant couples with no prior antiretroviral use were identified in a large referral center from February 2000 to January 2006 in southern Brazil. METHODS: Review of clinic records retrospectively identified 56 cases of untreated index cases whereas 37 couples were identified prospectively. Demographics, medical, and laboratory data were obtained. During follow-up, 41/93 index cases (44%) initiated antiretrovirals (ARVs) and from 52 without ARV use, 4 were lost to follow-up. Median viral loads were used to compare transmitters versus nontransmitters (Mann-Whitney test). RESULTS: Sixty-seven (72%) index cases were female (49% identified during ante-natal care). Unprotected sexual intercourse as a risk factor for HIV-1 infection was significantly higher as compared to intravenous drug use (P < 0.0001) in female index partners but not in male index cases. Sexually transmitted diseases were identified in 22 cases (24%). Six HIV-1 seroconversions occurred (6.5%). In all cases index partners were not using ARVs at the time of seroconversion. Among 26 couples with a male index case, there were 4 seroconversions (15%) and among 67 female index cases there were 2 seroconversions (3%). All seroconversions occurred with virus loads >1000 copies/mL. Eight female index cases (22%) reported no condom use. CONCLUSIONS: Heterosexual transmission occurred more frequently from HIV-infected males to females (rate ratio 3.5; CI, 95% 0.8-16.5 P = 0.259), although without statistical significance, probably because of the small sample. Transmitters showed significantly higher median viral loads (P = 0.042) suggesting that heterosexual transmission of HIV is more a function of viral load than gender of index case. ARV use may play a role in the prevention of HIV-1 heterosexual transmission. Other factors may be involved and should be further evaluated in larger cohorts.
J Acquir Immune Defic Syndr. 2002 Mar 1;29(3):275-83.
Male viral load and heterosexual transmission of HIV-1 subtype E in northern Thailand.
Tovanabutra S, Robison V, Wongtrakul J, Sennum S, Suriyanon V, Kingkeow D, Kawichai S, Tanan P, Duerr A, Nelson KE.
Research Institute for Health Sciences, Chiang Mai University, Chiang Mai, Thailand.
We evaluated the association between HIV-1 RNA copies/mL in men and heterosexual transmission to their female partners among 493 couples in Thailand. Husbands were identified as HIV-positive when they were screened as blood donors; nearly all were infected with HIV subtype E. Wives had no known risks for HIV infection other than sex with their husbands. In multivariate analysis, each log10 increment of HIV RNA in the man was associated with an 81% increased rate of HIV transmission to his wife (odds ratio = 1.81, 95% confidence interval: 1.33-2.48). No transmission occurred at viral loads below 1094 copies/mL, and a dose-response effect was seen with increasing viral load in the man. In multivariate analysis, a history of a sexually transmitted disease in the man or woman, longer duration of hormonal contraceptive use, and the woman's onset of sexual activity at less than 20 years of age were also associated with increased seropositivity of the wife.
J Virol. 2002 Jan;76(1):397-405.
Molecular epidemiology of human immunodeficiency virus type 1 transmission in a heterosexual cohort of discordant couples in Zambia.
Trask SA, Derdeyn CA, Fideli U, Chen Y, Meleth S, Kasolo F, Musonda R, Hunter E, Gao F, Allen S, Hahn BH.
Department of Medicine, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Most human immunodeficiency virus type 1 (HIV-1) transmissions in sub-Saharan Africa are believed to occur between married adults who are discordant for their HIV-1 infection status; however, no studies to date have investigated the molecular epidemiology of such transmission events. Here we report the genetic characterization of HIV-1 strains from 149 transmission pairs that were identified prospectively in a cohort of discordant couples in Lusaka, Zambia. Subgenomic gag, gp120, gp41, and/or long terminal repeat regions were amplified by PCR analysis of uncultured blood samples from both partners and sequenced without interim cloning. Pairwise genetic distances were calculated for the regions analyzed and compared to those of subtype-specific reference sequences as well as local controls. Sequence relationships were also examined by phylogenetic tree analysis. By these approaches, epidemiological linkage was established for the majority of transmission pairs. Viruses from 129 of the 149 couples (87%) were very closely related and clustered together in phylogenetic trees in a statistically highly significant manner. In contrast, viruses from 20 of the 149 couples (13%) were only distantly related in two independent genomic regions, thus ruling out transmission between the two partners. The great majority (95%) of transmitted viruses were of subtype C origin, although representatives of subtypes A, D, G, and J were also identified. There was no evidence for extensive transmission networks within the cohort, although two phylogenetic subclusters of viruses infecting two couples each were identified. Taken together, these data indicate that molecular epidemiological analyses of presumed transmission pairs are both feasible and required to determine behavioral, virological, and immunological correlates of heterosexual transmission in sub-Saharan Africa with a high level of accuracy.
AIDS Res Hum Retroviruses. 2001 Jul 1;17(10):901-10.
Virologic and immunologic determinants of heterosexual transmission of human immunodeficiency virus type 1 in Africa.
Fideli US, Allen SA, Musonda R, Trask S, Hahn BH, Weiss H, Mulenga J, Kasolo F, Vermund SH, Aldrovandi GM.
Department of Epidemiology and International Health, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
More than 80% of the world's HIV-infected adults live in sub-Saharan Africa, where heterosexual transmission is the predominant mode of spread. The virologic and immunologic correlates of female-to-male (FTM) and male-to-female (MTF) transmission are not well understood. A total of 1022 heterosexual couples with discordant HIV-1 serology results (one partner HIV infected, the other HIV uninfected) were enrolled in a prospective study in Lusaka, Zambia and monitored at 3-month intervals. A nested case-control design was used to compare 109 transmitters and 208 nontransmitting controls with respect to plasma HIV-1 RNA (viral load, VL), virus isolation, and CD4(+) cell levels. Median plasma VL was significantly higher in transmitters than nontransmitters (123,507 vs. 51,310 copies/ml, p < 0.001). In stratified multivariate Cox regression analyses, the risk ratio (RR) for FTM transmission was 7.6 (95% CI: 2.3, 25.5) for VL > or = 100,000 copies/ml and 4.1 (95% CI: 1.2, 14.1) for VL between 10,000 and 100,000 copies/ml compared with the reference group of <10,000 copies/ml. Corresponding RRs for MTF transmission were 2.1 and 1.2, respectively, with 95% CI both bounding 1. Only 3 of 41 (7%) female transmitters had VL < 10,000 copies/ml compared with 32 of 93 (34%) of female nontransmitters (p < 0.001). The transmission rate within couples was 7.7/100 person-years and did not differ from FTM (61/862 person-years) and MTF (81/978 person-years) transmission. We conclude that the association between increasing plasma viral load was strong for female to male transmission, but was only weakly predictive of male to female transmission in Zambian heterosexual couples. FTM and MTF transmission rates were similar. These data suggest gender-specific differences in the biology of heterosexual transmission.
J Acquir Immune Defic Syndr. 2001 Jul 1;27(3):277-80.
Mismatched human leukocyte antigen alleles protect against heterosexual HIV transmission.
Lockett SF, Robertson JR, Brettle RP, Yap PL, Middleton D, Leigh Brown AJ.
Centre for HIV Research, Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh, Scotland.
Genetic variation at the human leukocyte antigen (HLA) loci has been shown to be an important risk factor for progression to HIV disease, but its significance in infection is less well understood. We have investigated its role in HIV transmission in a cohort of individuals at risk for heterosexual infection. Analysis of over 80 individuals revealed that that the degree of concordance at HLA A, B, and DR loci differs significantly between transmitting and nontransmitting couples at risk for heterosexual HIV transmission (p <.02), suggesting that allogeneic immune responses may confer a degree of protection against HIV infection. Analysis of the frequencies of specific alleles at the A, B, and DR loci revealed a significantly higher frequency of HLA DR5 among exposed uninfected individuals, relative to population controls.
Lancet. 2001 Apr 14;357(9263):1149-53.
Probability of HIV-1 transmission per coital act in monogamous, heterosexual, HIV-1-discordant couples in Rakai, Uganda.
Gray RH, Wawer MJ, Brookmeyer R, Sewankambo NK, Serwadda D, Wabwire-Mangen F, Lutalo T, Li X, vanCott T, Quinn TC; Rakai Project Team.
Departments of Population and Family Health Sciences, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.
BACKGROUND: The probability of HIV-1 transmission per coital act in representative African populations is unknown. We aimed to calculate this probability overall, and to estimate how it is affected by various factors thought to influence infectivity. METHODS: 174 monogamous couples, in which one partner was HIV-1 positive, were retrospectively identified from a population cohort in Rakai, Uganda. Frequency of intercourse and reliability of reporting within couples was assessed prospectively. HIV-1 seroconversion was determined in the uninfected partners, and HIV-1 viral load was measured in the infected partners. Adjusted rate ratios of transmission per coital act were estimated by Poisson regression. Probabilities of transmission per act were estimated by log-log binomial regression for quartiles of age and HIV-1 viral load, and for symptoms or diagnoses of sexually transmitted diseases (STDs) in the HIV-1-infected partners. RESULTS: The mean frequency of intercourse was 8.9 per month, which declined with age and HIV-1 viral load. Members of couples reported similar frequencies of intercourse. The overall unadjusted probability of HIV-1 transmission per coital act was 0.0011 (95% CI 0.0008-0.0015). Transmission probabilities increased from 0.0001 per act at viral loads of less than 1700 copies/mL to 0.0023 per act at 38 500 copies/mL or more (p=0.002), and were 0.0041 with genital ulceration versus 0.0011 without (p=0.02). Transmission probabilities per act did not differ significantly by HIV-1 subtypes A and D, sex, STDs, or symptoms of discharge or dysuria in the HIV-1-positive partner. INTERPRETATION: Higher viral load and genital ulceration are the main determinants of HIV-1 transmission per coital act in this Ugandan population.
N Engl J Med. 2000 Mar 30;342(13):921-9.
Viral load and heterosexual transmission of human immunodeficiency virus type 1. Rakai Project Study Group.
Quinn TC, Wawer MJ, Sewankambo N, Serwadda D, Li C, Wabwire-Mangen F, Meehan MO, Lutalo T, Gray RH.
National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA.
BACKGROUND AND METHODS: We examined the influence of viral load in relation to other risk factors for the heterosexual transmission of human immunodeficiency virus type 1 (HIV-1). In a community-based study of 15,127 persons in a rural district of Uganda, we identified 415 couples in which one partner was HIV-1-positive and one was initially HIV-1-negative and followed them prospectively for up to 30 months. The incidence of HIV-1 infection per 100 person-years among the initially seronegative partners was examined in relation to behavioral and biologic variables. RESULTS: The male partner was HIV-1-positive in 228 couples, and the female partner was HIV-1-positive in 187 couples. Ninety of the 415 initially HIV-1-negative partners seroconverted (incidence, 11.8 per 100 person-years). The rate of male-to-female transmission was not significantly different from the rate of female-to-male transmission (12.0 per 100 person-years vs. 11.6 per 100 person-years). The incidence of seroconversion was highest among the partners who were 15 to 19 years of age (15.3 per 100 person-years). The incidence was 16.7 per 100 person-years among 137 uncircumcised male partners, whereas there were no seroconversions among the 50 circumcised male partners (P<0.001). The mean serum HIV-1 RNA level was significantly higher among HIV-1-positive subjects whose partners seroconverted than among those whose partners did not seroconvert (90,254 copies per milliliter vs. 38,029 copies per milliliter, P=0.01). There were no instances of transmission among the 51 subjects with serum HIV-1 RNA levels of less than 1500 copies per milliliter; there was a significant dose-response relation of increased transmission with increasing viral load. In multivariate analyses of log-transformed HIV-1 RNA levels, each log increment in the viral load was associated with a rate ratio of 2.45 for seroconversion (95 percent confidence interval, 1.85 to 3.26). CONCLUSIONS: The viral load is the chief predictor of the risk of heterosexual transmission of HIV-1, and transmission is rare among persons with levels of less than 1500 copies of HIV-1 RNA per milliliter.
J Infect Dis. 2000 Apr;181(4):1475-8. Epub 2000 Apr 7.
Virus load and risk of heterosexual transmission of human immunodeficiency virus and hepatitis C virus by men with hemophilia. The Multicenter Hemophilia Cohort Study.
Hisada M, O'Brien TR, Rosenberg PS, Goedert JJ.
Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20852, USA.
A high human immunodeficiency virus (HIV) load may increase the probability of HIV transmission by sexual contact, but the association of virus load of hepatitis C virus (HCV) with risk of HCV transmission is uncertain. HIV and HCV virus loads were examined in hemophilic men, as were risks of HIV and HCV transmission to their female partners in a hemophilia cohort in which most subjects are dually infected. A higher HIV load was associated with an increased risk of HIV transmission (odds ratio [OR], 1.31 per log10 increase in virus load). A higher HCV load was associated, although not significantly, with an increased risk of HCV transmission (OR, 1. 42 per log10). HCV load was higher among dually infected men than in those infected with HCV alone (P=.001). However, much larger studies are needed to clearly show whether HIV/HCV coinfection significantly increases the risk of HCV transmission to female partners.
J Acquir Immune Defic Syndr. 1999 Jun 1;21(2):120-5.
Heterosexual transmission of HIV-1 is associated with high plasma viral load levels and a positive viral isolation in the infected partner.
Pedraza MA, del Romero J, Roldán F, GarcÃa S, Ayerbe MC, Noriega AR, Alcamà J.
Servicio de Microbiologia, Centro de Investigación, Hospital 12 de Octubre, Madrid, Spain.
Risk factors for heterosexual HIV transmission are not fully understood. In fact, a proportion of people with sexual exposure to HIV remain uninfected despite multiple and continuous intercourse with HIV-infected partners. In this work, we have analyzed those virologic parameters potentially involved in the transmission of HIV through heterosexual contact. Thirty-eight couples with continuous unprotected sexual intercourse were included. HIV transmission occurred in 10 of 38 couples. No differences in clinical characteristics, exposure time, sexual practices, CD4 counts, or polymorphism in CCR5 were found between transmitter and nontransmitter groups. In contrast, virologic data were different between both groups; median values of viral load were 21.139 and 5.484 RNA copies/ml of plasma in the transmitter and nontransmitter groups, respectively, and a significant difference was found in mean viral load values (p = .03, Mann-Whitney test). Viral isolation was obtained in 90% of transmitters, but in only 44% of nontransmitter subjects (p = .02, Fisher's exact test). These data show that viral load levels and a positive viral isolation in culture must be considered as risk factors for heterosexual transmission of HIV-1.
AIDS. 1999 Jun 18;13(9):1083-9.
Rates of HIV-1 transmission within marriage in rural Uganda in relation to the HIV sero-status of the partners.
Carpenter LM, Kamali A, Ruberantwari A, Malamba SS, Whitworth JA.
Medical Research Council Programme on AIDS, Uganda Virus Research Institute, Entebbe.
OBJECTIVE: To assess the efficacy of transmission of HIV-1 within married couples in rural Uganda according to the sero-status of the partners. DESIGN: Estimation of HIV incidence rates for 2200 adults in a population cohort followed for 7 years comparing male-to-female with female-to-male transmission and sero-discordant with concordant sero-negative couples. METHODS: Each year, adults (over 12 years of age) resident in the study area were linked to their spouses if also censused as resident. The HIV sero-status was determined annually. RESULTS: At baseline 7% of married adults were in sero-discordant marriages and in half of these the man was HIV-positive. Among those with HIV-positive spouses, the age-adjusted HIV incidence in women was twice that of men (rate ratio (RR) = 2.2 95% confidence interval (CI) 0.9-5.4) whereas, among those with HIV-negative spouses, the incidence in women was less than half that of men (RR = 0.4, 95% CI 0.2-0.8). The age-adjusted incidence among women with HIV-positive spouses was 105.8 times (95% CI 33.6-332.7) that of women with HIV-negative spouses, the equivalent ratio for men being 11.6 (95% CI 5.8-23.4). CONCLUSION: Men are twice as likely as women to bring HIV infection into a marriage, presumably through extra-marital sexual behaviour. Within sero-discordant marriages women become infected twice as fast as men, probably because of increased biological susceptibility. Married adults, particularly women, with HIV-positive spouses are at very high risk of HIV infection. Married couples in this population should be encouraged to attend for HIV counselling together so that sero-discordant couples can be identified and advised accordingly.
J Acquir Immune Defic Syndr Hum Retrovirol. 1998 Jan 1;17(1):42-5.
Heterosexual HIV-1 transmission and viral load in hemophilic patients.
Ragni MV, Faruki H, Kingsley LA.
Department of Medicine, University of Pittsburgh School of Medicine and The Hemophilia Center of Western Pennsylvania, 15213-4306, USA.
Only one fifth or fewer of the female sexual partners of HIV-1-infected men with hemophilia become infected. The risk factors associated with heterosexual transmission of HIV-1 are not well understood. To investigate the hypothesis that HIV-1 viral load may be related to heterosexual HIV-1 transmission, we measured HIV-1 RNA by polymerase chain reaction (PCR) in frozen samples from 39 men with hemophilia and HIV-1 infection obtained between 20 and 62 months after HIV-1 seroconversion, during at least a 6-month relationship with a female sexual partner. The median time from the hemophilic viral load determination to the estimated date of transmission to the female partner was 9 months (range, 4-41 months). The proportion of HIV-positive hemophilic men with over 100,000 HIV RNA copies/ml was significantly higher in transmitters (TR) (3 of 5 [60%]), than in nontransmitters (NTR) (3 of 34 [9%]; p = 0.027). There were no differences between TR and NTR in age at seroconversion (32.4 years each), in time from seroconversion to AIDS (67 versus 79 months), in mean CD4 number (245/microl] versus 260/microl); nor in the proportion who developed AIDS (4 of 5 [80%] versus 24 of 34 [71%]). These findings appear to suggest that high HIV viral load in HIV-infected hemophilic men increases the risk of HIV transmission to heterosexual partners. Viral load determinations may be helpful in counseling hemophilic couples regarding transmission to female partners.
Am J Epidemiol. 1997 Oct 15;146(8):655-61.
Role of viral load in heterosexual transmission of human immunodeficiency virus type 1 by blood transfusion recipients. Transfusion Safety Study Group.
Operskalski EA, Stram DO, Busch MP, Huang W, Harris M, Dietrich SL, Schiff ER, Donegan E, Mosley JW.
Department of Medicine, University of Southern California, Los Angeles, USA.
Eighteen transfusion recipients infected with human immunodeficiency virus type 1 (HIV-1) were followed prospectively with their 19 long-term sexual partners from 1986 to 1993 in California, Florida, and New York. Follow-up included clinical, behavioral, immunologic, serologic, and virologic evaluations. Two partners were already infected when seen 18 and 34 months after sexual contact began following the infectious transfusion. Four of 17 initially seronegative partners seroconverted during 23 person-years of observation. The recipient's clinical status, mononuclear cell subset variations, and time trend in CD4+ counts had no association with transmission. Individual plasma HIV-1 ribonucleic acid (RNA) loads were stable during observation, and sexual transmission was not attributable to an upward trend or transient burst in viremia. However, recipients who transmitted HIV-1 to their sexual partners had higher mean viral RNA levels than did nontransmitting recipients (4.3 vs. 3.6 log10 copies/ml; p = 0.05). Although this series was small, the prospective observations suggest that viral load was the only characteristic in the recipient that contributed to heterosexual infectiousness.
AIDS. 1997 Jul 15;11(9):1089-94.
Biological correlates of HIV-1 heterosexual transmission.
Fiore JR, Zhang YJ, Björndal A, Di Stefano M, Angarano G, Pastore G, Fenyö EM.
Microbiology and Tumorbiology Centre, Karolinska Institute, Stockholm, Sweden.
OBJECTIVES: To study the role of HIV-1 biological phenotype, viral load and neutralizing antibodies in male-to-female heterosexual transmission of HIV-1. METHODS: Seven transmitting and seven non-transmitting HIV-1-seropositive heterosexual male index cases were included in the present study. All couples had engaged in unprotected sex for a period of over 1 year. Transmission was defined by the seroconversion of the female sexual partner. Virus isolates were tested in MT-2 cells for replication and syncytia induction. HIV-1 RNA plasma load was measured by the branched DNA technique. Serum neutralizing activity to primary HIV-1 isolates was tested by using peripheral blood mononuclear cells (PBMC) as target cells. RESULTS: Non-transmitting index cases had a lower HIV-1 RNA concentration in plasma than transmitting index cases. Non-transmitting index cases also tended to have serum neutralizing activity with broad specificity and to have viruses with low replicative capacity, as characterized by 50% infectious dose titres in PBMC and by the lack of MT-2 tropism. CONCLUSIONS: The results indicate that plasma viral-RNA load is a marker for transmission. Moreover, an interplay between the host immune response and viral replication may modulate the level of viral load and thereby influence HIV-1 transmission.
Ann Intern Med. 1996 Aug 15;125(4):324-30.
Heterosexual transmission of HIV in Haiti.
Deschamps MM, Pape JW, Hafner A, Johnson WD Jr.
Cornell University Medical College, New York, New York, USA.
BACKGROUND: Despite the importance of human immunodeficiency virus (HIV) transmission through heterosexual contact, the incidence of HIV infection in heterosexual cohorts has not been well studied, particularly in the developing world. OBJECTIVE: To 1) determine the incidence of HIV infection in discordant heterosexual couples (couples in which one partner had HIV infection and the other did not) in Haiti and 2) assess risk factors for and methods of preventing HIV infection. DESIGN: Prospective study. SETTING: National Institute for Laboratory Research, Portau-Prince, Haiti. PARTICIPANTS: 475 HIV-infected patients and their noninfected regular sex partners. MEASUREMENTS: Patients and their partners were evaluated at 3- to 6-month intervals for HIV infection, sexually transmitted diseases, and sexual practices. The efficacy of counseling and provision of free condoms was also evaluated. RESULTS: Among the 177 couples who remained sexually active during the prospective study period, 20 seroconversions to HIV positivity occurred, for an incidence rate of 5.4 per 100 person-years (95% CI, 5.16 to 5.64 per 100 person-years). Thirty-eight couples (21.5%) discontinued sexual activity during the study. Only 1 seroconversion occurred among the 42 sexually active couples (23.7% of the 177 sexually active couples) who always used condoms. In contrast, the incidence in sexually active couples who infrequently used or did not use condoms was 6.8 per 100 person-years (CI, 6.49 to 7.14 per 100 person-years). Transmission of HIV was associated with genital ulcer disease, syphilis, and vaginal or penile discharge in the HIV-negative partner and with syphilis in the HIV-infected partner. CONCLUSION: Counseling and the provision of free condoms contributed to the institution of safe sex practices or abstinence in 45% of discordant heterosexual couples. However, 55% of couples reported that they continued to have unprotected sex, resulting in an incidence of HIV infection of 6.8 per 100 person-years.
Infection. 1995 Jan-Feb;23(1):29-32.
Male-to-female transmission of HIV in a cohort of hemophiliacs--frequency, risk factors and effect of sexual counseling.
Rockstroh JK, Ewig S, Bauer T, Lüchters G, Oldenburg J, Bailly E, Kaiser R, Schneweis KE, Brackmann HH, Dengler HJ, et al.
Medizinische Universitätsklinik und Poliklinik, Bonn, Germany.
The incidence of male-to-female transmission of HIV infection was studied in a population of 198 sexual partners of hemophiliacs who tested HIV positive since 1984. The follow-up observation period was 1987-1992. Transmission occurred in 20 (10%) cases. The analysis of risk factors for transmission was performed in a subgroup of 57 hemophiliacs with seronegative sexual partners as compared to eight transmitters. Transmitters showed a significantly more advanced immune depletion at enrollment as well as at the end of the observation period. Furthermore, transmitters had a more advanced disease at the end of the study (75% vs. 29% CDC IV; p < 0.01). Also virus cultures were more frequently positive in the transmitters than in the non-transmitters (71% vs. 42%). Regular sexual counseling was offered to all couples. After 1987, no new seroconversions were detected. However, two seroconversions in female partners of hemophiliacs outside the initial study population were observed. Both transmissions occurred during a period of severe clinical and immunological deterioration. This study shows that sexual partners of HIV-infected hemophiliacs with more advanced disease are at higher risk of infection with HIV. The frequency of male-to-female transmission of HIV in long-term monogamous sexual relationships practicing safer sex is low. Overall, disease awareness and counseling for safer sex seem to be effective in reducing transmission rates.
Epidemiology. 1994 Nov;5(6):570-5.
The efficiency of male-to-female and female-to-male sexual transmission of the human immunodeficiency virus: a study of 730 stable couples. Italian Study Group on HIV Heterosexual Transmission.
Nicolosi A, Corrêa Leite ML, Musicco M, Arici C, Gavazzeni G, Lazzarin A.
Department of Epidemiology and Medical Informatics, National Research Council, Milan, Italy.
To compare the efficiency of male-to-female and female-to-male sexual transmission of human immunodeficiency virus (HIV), we studied 524 female partners of HIV-infected men and 206 male partners of HIV-infected women in 16 Italian clinical centers. All of the partners had had a sexual relationship with the index case lasting for at least 6 months and presented no other risk factor than sexual exposure to the HIV-infected partner. Among the 730 couples, 24% of the female partners were HIV positive, in comparison with 10% of the male partners. Using logistic regression analysis, including gender and controlling for condom use, frequency of intercourse, anal sex, partner's CD4+ cell count and clinical stage, sexually transmitted diseases, genital infections, and contraceptive use, we found that the efficiency of male-to-female transmission was 2.3 (95% confidence interval = 1.1-4.8) times greater than that of female-to-male transmission. Between-gender differences in the contact surfaces and the intensity of exposure to HIV during sexual intercourse are possible reasons for the difference in efficiency of transmission.
N Engl J Med. 1994 Aug 11;331(6):341-6.
A longitudinal study of human immunodeficiency virus transmission by heterosexual partners. European Study Group on Heterosexual Transmission of HIV.
de Vincenzi I.
European Centre for the Epidemiological Monitoring of AIDS, Hôpital National de Saint-Maurice, France.
BACKGROUND. Worldwide, the predominant mode of human immunodeficiency virus (HIV) transmission is heterosexual intercourse, but the risk of heterosexual transmission and the effectiveness of measures to prevent it are not well defined. METHODS. We conducted a prospective study of HIV-negative subjects whose only risk of HIV infection was a stable heterosexual relationship with an HIV-infected partner. Every six months the subjects were interviewed, tested for HIV, and counseled about safe sexual practices. RESULTS. A total of 304 HIV-negative subjects (196 women and 108 men) were followed for an average of 20 months. During the study, 130 couples (42.8 percent) ended their sexual relationships, most often because of the HIV-infected partner's illness or death. Of the 256 couples who continued to have sexual relations for more than three months after enrollment in the study, only 124 (48.4 percent) used condoms consistently for vaginal and anal intercourse. Among these couples, none of the seronegative partners became infected with HIV, despite a total of about 15,000 episodes of intercourse. Among the 121 couples who used condoms inconsistently, the rate of seroconversion was 4.8 per 100 person-years (95 percent confidence interval, 2.5 to 8.4). Eleven couples refused to answer questions about condom use. The risk of transmission increased with advanced stages of HIV infection in the index partners (P < 0.02) and with genital infection in the HIV-negative partners (P < 0.04). Withdrawal to avoid ejaculation in the vagina had a protective effect in uninfected women (P < 0.02). CONCLUSIONS. Consistent use of condoms for heterosexual intercourse is highly effective in preventing the transmission of HIV. Among couples not using condoms regularly, the risk of HIV transmission varies widely.
J Acquir Immune Defic Syndr. 1993 May;6(5):497-502.
Man-to-woman sexual transmission of HIV: longitudinal study of 343 steady partners of infected men.
Saracco A, Musicco M, Nicolosi A, Angarano G, Arici C, Gavazzeni G, Costigliola P, Gafa S, Gervasoni C, Luzzati R, et al.
Epiunit, HIV Center, IRCCS Ospedale San Raffaele, Milano, Italy.
To study incidence and risk factors of heterosexually transmitted HIV infection, we followed a cohort of 343 seronegative women, stable, monogamous partners of infected men whose only risk of acquiring HIV was sexual exposure to the infected partner. Nineteen seroconversions occurred in 529.6 person years (py) of observation, yielding an incidence rate of 3.6 per 100 py. The incidence rate was 7.2 per 100 py among women who did not always use or never used condoms and 1.1 among those who always used them [relative risk (RR) 6.6, 95% confidence interval (CI) 1.9-21.9]. Anal sex was associated with a risk increase in only those women not always using condoms (RR 1.4, 95% CI 0.4-4.8). No seroconversions were observed among 22 women using oral contraceptives. One of the women using intrauterine devices seroconverted. In couples who did not always use condoms, seroconversions occurred more frequently in partners of men with symptomatic diseases, with a low CD4+ cell number (< 400 per mm3) or with a detectable p24 antigen. In couples not always using condoms and where the man had a low CD4+ cell count, the joint presence of blood viral antigens and AIDS symptoms conditioned a fivefold increased risk of seroconversion of the woman (RR 5.4, CI 1.4-20.3). At multivariate analysis, women with longer relationships (> or = 1 year) showed a lower risk of seroconversion (RR 0.3, CI 0.1-0.8), and those partners of men positive for p24 antigen in serum had an increased risk of seroconversion (RR = 4.0, CI 0.1-0.8).
BMJ. 1992 Mar 28;304(6830):809-13.
Comparison of female to male and male to female transmission of HIV in 563 stable couples. European Study Group on Heterosexual Transmission of HIV.
OBJECTIVE--To identify risk factors for heterosexual transmission of HIV and to compare the efficiency of male to female and female to male transmission. DESIGN--Cohort study of heterosexual couples. Regular partners of HIV infected subjects were tested and both members of the couples interviewed every six months. HIV prevalence in partners was analysed according to the characteristics of the couples. SETTING--Nine European countries. SUBJECTS--563 couples comprising 156 female index patients with their 159 male partners and 400 male index patients with their 404 female partners. Partners reporting risk factors other than sexual contacts with the index patient were excluded. MAIN OUTCOME MEASURES--HIV infection in partners and high risk sexual behaviour. RESULTS--Overall, 19 (12%) male partners and 82 (20%) female partners were infected with HIV, suggesting that male to female transmission is 1.9 (95% confidence interval 1.1 to 3.3) times more effective than female to male transmission. An advanced stage of HIV infection in the index patient (odds ratio 17.6; 4.9 to 62.7) and sexual contacts during menses (3.4; 1.0 to 11.1) increased the risk of female to male transmission and stage of infection (2.7; 1.5 to 4.9), anal sex (5.1; 2.9 to 8.9), and age of the female partner (3.9; 1.2 to 13.0 for age over 45 years) increased the risk of male to female transmission. None of the 24 partners who had used condoms systematically since the first sexual contact was infected. CONCLUSIONS--Several factors which potentiate the risk of transmission through unprotected vaginal intercourse have been identified. Knowledge of these factors could be helpful for counselling patients infected with HIV and their sexual partners.
BMJ. 1992 Jun 20;304(6842):1605-9.
Effect of serotesting with counselling on condom use and seroconversion among HIV discordant couples in Africa.
Allen S, Tice J, Van de Perre P, Serufilira A, Hudes E, Nsengumuremyi F, Bogaerts J, Lindan C, Hulley S.
Department of Pathology, University of California, San Francisco.
OBJECTIVE--To determine whether HIV testing and counselling increased condom use and decreased heterosexual transmission of HIV in discordant couples. DESIGN--Prospective study. SETTING--Kigali, the capital of Rwanda. SUBJECTS--Cohabiting couples with discordant HIV serology results. MAIN OUTCOME MEASURES--Condom use in the couple and HIV seroconversion in the negative partners. RESULTS--60 HIV discordant couples were identified, of whom 53 were followed for an average of 2.2 years. The proportion of discordant couples using condoms increased from 4% to 57% after one year of follow up. During follow up two of the 23 HIV negative men and six of the 30 HIV negative women seroconverted (seroconversion rates of 4 and 9 per 100 person years). The rate among women was less than half that estimated for similar women in discordant couples whose partners had not been serotested. Condom use was less common among those who seroconverted (100% v 5%, p = 0.01 in men; 67% v 25%, p = 0.14 in women). CONCLUSIONS--Roughly one in seven cohabiting couples in Kigali have discordant HIV serological results. Confidential HIV serotesting with counselling caused a large increase in condom use and was associated with a lower rate of new HIV infections. HIV testing is a promising intervention for preventing the spread of HIV in African cities.
Cooler,
"You guys can add the Padian study to this list where there was no seroconversions in thousands of instances of serodiscordant couples having all kinds of sex."
Do a bit of research before you misquote/misunderstand/regurgitate denialist crap. Padian herself commented on those idiots who would misquote her saying (among other things):
That we witnessed no HIV transmissions after the intervention documents the success of the interventions in preventing the sexual transmission of HIV. The sentence in the Abstract reflects this success â nothing more, nothing less. Any attempt to refer to this or other of our publications and studies to bolster the fallacy that HIV is not transmitted heterosexually or homosexually is a gross misrepresentation of the facts and a travesty of the research that I have been involved in for more than a decade.
Some of those abstracts got truncated, but you can read the full versions in PubMed: http://www.ncbi.nlm.nih.gov/sites/entrez
Also, I just saw this study, which shows that transmission can be quite efficient under some circumstances.
Swiss Med Wkly. 2009 Apr 4;139(13-14):207-9.
Unusually high HIV infectiousness in an HIV-, HCV- and HSV-2-coinfected heterosexual man.
Witteck A, Yerly S, Vernazza P.
Department of Infectious Diseases, Cantonal Hospital, St. Gallen, Switzerland.
We report an HIV-HCV-HSV-2-coinfected man, who infected all of five sequential female sexual partners within seven years. HIV-RNA in semen was unusually high and exceeded that in plasma by one log10. Screening for sexually transmitted diseases remained negative with the exception of HSV-2-seropositivity. Recurrent asymptomatic genital herpes might explain the patient's increased HIV-RNA shedding in semen.
I make no claim as to know who and how many may have killed JFK. You claim the US Governement is lying and that Harvey didn't act alone.
Prove it.
Every time someone asks you for evidence, you tell them to go provide oral stimulation on someone's genitalia, but can provide no evidence. I not you still have an unhealthy fixation on other people's intimate organs. You should see a mental health specialist about that.
You are making claims, so you must provide the evidence.
thankss.
Thanks for evading the issue. I've already given evidence of why I am skeptical of the JFK theory.(Back and to the left)I do not know exactly what happened, but A congressional Inquiry in 1973 stated there was more than one shooter, and 70% of Americans doubt the official theory. I would support another investigation. I can't give a full narrative of events of what happened, this is only possible with a real investigation soon after the fact. Sadly many witnesses Garrison called mysteriously died, making even a legitamate investigation difficult.
The DA's office in New Orleans led by Jim Garrison provided a lot of paradoxes that make the official theory implausable. This is what Oliver Stones film JFK is based upon. It is not my problem if you guys are too dumb and narrow minded to have seen the film, even though it has some great actors like Kevin Costner, Joe Pesci, Kevin Bacon and Tommy Lee Jones. It is not my fault that you guys are weirdos and would rather stare and obsess over mediocre scientists that look like neandertherals like PZ Myers and also have a boycrush on Orac, a guy that is like 60 years old and still talks about Battlestar Gallatica, instead of wanting to watch a thought provoking film like JFK.
If you have not read any of these investigations you should not have an opinion since you are totally uneducated on the subject. Nevertheless since you guys think anybody that questions these theories are "nuts" answer some questions.
I'd like the overwhelming evidence Lee Harvey Oswald acted alone and that there were not other shooters involved.
Overwhelming evidence 19 hijackers were at the airports(videos of all of them etc.)
Overwhelming evidence that HIV was a fatal disease that Justified AZT's release in 1987 and the DHHS saying the probable cause of AIDS was HIV in 1984 and the IOM recommending billions in funding in 1985. When you cite papers please describe how they proved HIV was a fatal disease for the significant majority who were infected. Waiting.
I make no claim as to any of the above. You and your ilk claim the scientific community is lying to the public about the origin of AIDS. You claim they are paid by the pharmaceutical industry to push unneeded drugs. You make all these claims, so you must provide the evidence. When someone cries wolf, there better be a wolf. Otherwise that makes you a crank.
You claim Harvey did not act alone, provide evidence for that. (I saw JFK, by the by, good fun entertainment. Not evidence) I did not claim there were 19 hijackers. But you claim the US government brought the towers down. Provide evidence.
You want people to listen to you, then try convincing them.
I'm a member of the public you seem so determined to save from the evil plans of the dastardly Frankensteins in the pay of the Great Pharma who aim to take over the world, bla bla bla.....
Someone comes along and tells me that "they" are cheating, lying, stealing, plotting, being devious, etc... (pick your favorite.)
I say: really? Tell me more.
He says: They are lying to you.
I say: prove it.
He says: go suck on shickaling's balls
I say: Oh well, another crank
Thanks for not answering a single question. Bye Bye gotta go.
Pack lots of coolaid and tinfoil. Don't go too far, you might fall off the edge of the world. Cheerio!
"If you have not read any of these investigations you should not have an opinion since you are totally uneducated on the subject."
Cooler, i second that and apply it to you. If you haven't read/understood the papers on HIV then kindly shut your trap as you likewise should not have an opinion on it. Since we both agree on this can we assume you won't be posting your nonsense here anymore?
Poodle,.............."the best we can do is take an educated guess. So you watched the movie? Tell me what the rest of his quotation linked to this was. Tell us the context and the question asked."
Yes please an educated guess. I have to see it again to tell you precisely, but you can go see it yourself too.
Carter,
An educated guess was already given by DT. It is pretty much the same as what I would guess without knowing the full context of the conversation.
As for watching the movie, sorry but I have no plans to do so. It looks to be nothing more than the same denialist cherry picking and BS that has been debunked over and over. Any movie portraying the Perth Group as reliable authorities isn't worth my time as it is clearly biased and not based in anything remotely related to reality. House of cards seems just as grounded in reality as Charlie and the Chocolate Factory.
Perhaps you can also answer NM's question as to how Joe Mandinski is doing since you moderated along side him on AME for so long.
Carter, you asked this question:
"Question: If Luc Montagnier says, " We can be exposed many times to HIV without having been infected and our immune system can get ride of the virus in a few weeks if you have a good immune system", wouldn't that mean that HIV is a result of immune deficiency and not the other way around as we've been forced fed to believe?"
This has been answered - no. See the studies of exposed seronegatives posted above for the reality of what Montagnier was talking about (as opposed to your delusional fantasy). I think it's wonderful that AIDS denialists have their own version of Expelled, I remember the ID message boards being abuzz about how that movie was going to challenge evolution science and boy have those predictions come true! Duping scientists into participating in crappy propaganda was really an excellent model to follow!
Related to the issue of Joe Mandinski's health I would like to point out studies show that most HIV+ individuals with symptomatic toxoplasmosis infection already have CD4 counts below 100 cells/ml. Perhaps it is time for him to follow some real medical advice instead of the same old pseudoscience crap on AME.
A humorous aside while we wait for Carter to return, wikipedia has a quote about the Expelled (Intelligent Design) movie:
Its selling point is that academic freedom in the US is threatened by a vast conspiracy of atheist scientists, hypnotised by what Stein labels in the film the "Darwinian gospel." Supporters of ID are fired from their institutions or denied tenure, the film argues, while journalists who report on ID are silenced or shunned. This is an old trick. By claiming their views are suppressed, proponents of ID hope to be protected from criticism. When someone argues that ID is bogus, all they need do is yell: "See? Suppression!"
If we replace the 5 bolded terms to:
Its selling point is that academic freedom in the US is threatened by a vast conspiracy of atheist scientists, hypnotised by what Duesberg labels in the film the "AIDS gospel." Denialists are fired from their institutions or denied tenure, the film argues, while journalists who report on AIDS denialism are silenced or shunned. This is an old trick. By claiming their views are suppressed, proponents of denialism hope to be protected from criticism. When someone argues that AIDS denialism is bogus, all they need do is yell: "See? Suppression!"
we have what is probably a pretty good summary of the House of Cards movie! Coincidence?
Sorry folks, but contrary to your popular belief the Film House of Numbers is not a so called dissident film. It's a journey that reveals several sides of the AIDS saga, leaving it up to the viewer to form their own opinion.
Then why might you ask, why are we witnessing the dissidents standing behind this film. The answer is because it's a balanced look at the problem. Ah, but then again your lot doesn't think you have a problem.
Carter,
"Then why might you ask, why are we witnessing the dissidents standing behind this film. The answer is because it's a balanced look at the problem. Ah, but then again your lot doesn't think you have a problem."
Any movie portraying the Perth Group as credible authorities on HIV is by no means balanced. Does the movie provide the balanced view that they were both denied as expert witnesses in court on more than one occassion because that have NO EXPERTISE in the field of HIV biology? No? A balanced movie would do that. Heck, even the 2 minute trailer for it makes it more than clear it is just another denialist propaganda film. Unbiased would require an understanding of biology; something 99.99% of denialists do not have.
That we are witnessing denialists "standing behind this film" is all the more evidence that this is no unbiased documentary, as denialists as a whole cling to anything they believe supports their faith at the expense of the facts that don't.
Any news on Joe? I noticed you didn't mention him in your last post.
"A balanced movie would do that."
No your mistakern, because this is a narrow one sided view held by you and yours.
I have no information about Joe. You'll have to look elsewhere and when you do I'm sure it will also stick to a narrow one sided view.
Notice how the assorted nutcases like poodle stomper, Chris Noble, Srsly, NM et al can't answer a single question. All they can do is spam a website, something that would get you laughed out of a courtroom and flunk you out of any debate class. Here is one question that the crackpots can't answer.
Pleaase provide the Overwhelming evidence that HIV was a fatal disease that Justified AZT's release in 1987 and the DHHS saying the probable cause of AIDS was HIV in 1984 and the IOM recommending billions in funding in 1985. When you cite papers please describe how they proved HIV was a fatal disease for the significant majority who were infected. Waiting.
So it's a "narrow one sided view" to think that a hospital technician and emergency room from Perth, who have never conducted any scientific research, aren't the best people to promulgate rules of viral isolation? I think that is rational. People outside of Australia don't seem to appreciate just how much of a national joke the Parenzee case made those two.
Any more to offer on that Montagnier quote, carter?
No NM. You'll have to go see the film yourself.
Yes, it is very one sided, steeped in propaganda view that you and ilk so desperatly cling to. Correction: Biophysicist Eleni Papadopulos-Eleopulos http://www.theperthgroup.com/Parenzee.html
So your earlier attempt at a rhetorical triumph:
"wouldn't that mean that HIV is a result of immune deficiency and not the other way around as we've been forced fed to believe?"
has now been abandoned, as the only thing you exposed was your ignorance.
Eleni Papadopulos-Eleopulos is a hospital technician who tests patients for sensitivity to UV radiation. Denial is a great market for people like that who are great scientists in their own mind (cf Henry Bauer), they know that their audience will accept and defend anything they say. Won't they, carter?
Carter,
"No your mistakern, because this is a narrow one sided view held by you and yours."
One sided? How many judges said that they were basically incompetent to testify as expert witnesses? You call this one-sided? Let me ask a few other things then.
A) Does the film cite Mullis? If it does does it also mention that he believes he has been abducted by aliens or that sees glowing raccoons?
B) Does it quote Duesberg? Does it also mention that he demolished his own career in cancer research when he decided that only his strict aneuploidy theory could explain cancer?
C) Does the film mention Alive and Well? If it does, did it also mention that desseminated herpes and multiple bouts of pneumonia are not typical of stressed people (TV or no TV)?
D) Does it mention that Continuum shut down when it's HIV+ editorial staff all died?
E) Does it mention that another HIV+ AME moderator died of what doctors defined as AIDS?
F) Does it mention that HIV+ denialists die of "mysterious" (i.e. AIDS-defining) illnesses while those who are HIV- seem surprisingly resistant to this? Does it mention how the HIV+ denialists are dying disproportionately to those who are not?
Tell me does the film mention any of these or is that not "balanced" enough?
"I have no information about Joe. You'll have to look elsewhere and when you do I'm sure it will also stick to a narrow one sided view."
I'm curious then, have you already begun thinking of excuses for his passing? Have you begun rationalizing why someone would develop symptomatic toxoplasmosis (rarely ever seen in immunocompetent individuals) if he were perfectly healthy and HIV were harmless/nonexistent? How many friends will you have to bury before you pull your head out of your ass and realize that you helped further their faith in the BS that you preach?
Letâs see what the judge said about the two Perthers:
On Elenei:
Ms Papadopulos-Eleopulos has no practical experience. She has never worked with patients who are said to be infected with HIV, or with any virus. She has never treated or diagnosed patients who have viruses. She has never worked in laboratories or conducted research. She has no practical experience.
She has given evidence on the topics of virology, immunology, epidemiology, microbiology and microscopy. She has no practical experience and she has never worked in any of the areas.
Although Ms Papadopulos-Eleopulos demonstrated a superficial understanding of a number of the areas, I consider that her knowledge is limited to her reading. She has what one might describe as a textbook understanding of the science of viruses, but she has no depth of knowledge or understanding and she simply relies upon written material. She did not demonstrate any understanding or knowledge similar to that demonstrated by the witnesses called by the DPP.
I conclude that she does not have expertise in the various disciplines in which expertise is required. In my opinion, she is not qualified to express opinions about the existence of HIV, or whether it has been established that it causes AIDS. Nor has she expertise to express opinions about whether the virus is transmissible. Nor is she qualified to express opinions about the tests that have been developed to diagnose the virus.
On Turner:
I conclude that Dr Turner is not qualified to advance expert opinion about virus isolation, antibody tests, viral load tests, or sexual transmission of the virus. His knowledge of these subjects is limited to having read a number of publications. He relies entirely on his interpretation of various studies in the specialized disciplines of virology, epidemiology, microbiology, immunology, pathology or infectious diseases, in none of which he has qualifications beyond his medical degree. He has no practical experience, and has performed no research which has been published.
Are you saying that a balanced film should use them as authorities but should not bother mentioning this? Who exactly do you think you're fooling. This is clearly denialist propaganda and in no way balanced.
Next thing you know, they'll be citing Hank Barnes as a legal authority...
I am looking forward to seeing House of Numbers, the documentary that critques the mainstream AIDS view:
http://www.houseofnumbers.com/
Here's a short movie review from the Tennessean:
http://www.tennessean.com/article/20090414/ENTERTAINMENT0403/90414019
Unfortunately, like all other denialist movies, this promises nothing more than cherry-picked phrases, biased so-called "authorities", and a complete lack of critical thinking. I highly doubt it will even bother to mention all the denialists that have died from AIDS-defining illnesses. No problem, though. The denialists will watch it and nod vacant-eyed in agreement at all the things that confirms their preconceived beliefs while the HIV+ denialists continue to die and the HIV- ones continue to live (mysteriously).
One of the most disturbing quotes from the movie (according to the review) is:
But one of the most poignant, revealing moments of House of Numbers is Leungâs interview with a South African woman.
âA lot of people here is very sick and is very dying,â she said.
âWhat kind of sickness do you see around here?â Leung asks.
âItâs HIV/AIDS,â she explains.
âWhat is AIDS?â Leung asks.
With frustration, and a shrug of the shoulders, she exclaims, âWe donât know. We donât know!â
Huh. So an average run-of-the-mill African civilian they interviewed didn't know much about the biology of AIDS? This is why educational programs are targeted towards them. I'm not sure what this moment is meant to "reveal" other than most people in developing countries are not well versed in virology. Most people in developing countries aren't either. This is no surprise.
Poodle Stomper, you sound like a deranged immature fellow.
Why not open your eyes a bit, and apply a little science?
Ah but my eyes are open. I have read enough denialist crap to know what to expect but I'll tell ya what "Freddy", how about you take a stab at what I asked Carter about the movie:
A) Does the film cite Mullis? If it does does it also mention that he believes he has been abducted by aliens or that he claimed to have seen glowing raccoons?
B) Does it quote Duesberg? Does it also mention that he demolished his own career in cancer research when he decided that only his strict aneuploidy theory could explain cancer?
C) Does the film mention Alive and Well? If it does, did it also mention that desseminated herpes and multiple bouts of pneumonia are not typical of stressed people (TV or no TV)?
D) Does it mention that Continuum shut down when it's HIV+ editorial staff all died?
E) Does it mention that another HIV+ AME moderator died of what doctors defined as AIDS?
F) Does it mention that HIV+ denialists die of "mysterious" (i.e. AIDS-defining) illnesses while those who are HIV- seem surprisingly resistant to this? Does it mention how the HIV+ denialists are dying disproportionately to those who are not?
G) Do they cite the Perth Group as authorities (clearly from the trailer they did)? If so, did they also mention that they have been deemed not competent to serve as expert witnesses because, like every other denialist, they have no expertise with HIV?
Poodle Stomper,
Instead of reciting stale talking points, why not apply some SCIENCE?
Obviously, the retroviral theory of causation is falsifiable (or else it wouldn't be science). So, what evidence would falsify your belief that AIDS is caused by a solitary retrovirus?
This really isn't hard -- except for the emotions that cloud your mind.
Freedy,
AIDS is not caused by a "solitary retrovirus". HIV-1 and HIV-2 can and do both cause AIDS in humans. Even within HIV-1 there are 3 groups and many subtypes within the M group.
There are many types of evidence that could falsify the belief that HIV-1 and HIV-2 are the causes of AIDS, but so far no such evidence has been found. The arguments against HIV are just hot air, no data or evidence behind them.
"So, what evidence would falsify your belief that AIDS is caused by a solitary retrovirus?"
The unmistakable Hank Barnes. Hank, if you follow 175 couples for a total of 282 couple-years of follow-up, how long have you followed each couple on average?
"Freddy",
"Instead of reciting stale talking points, why not apply some SCIENCE?"
Stale? None of those points have been answered yet. You are the one who brought up the film and it's review. I am just asking if it is truly as balanced as Carter claimed. Since you seem to be supportive of the movie (and you claim you support science) don't you agree that a film promoted as informative should in fact inform from reliable authority rather than pseudoscience? If it uses authorities denied from testifying in court due to having no expertise in the field, isn't this something it should also inform the viewers? What's the matter? Suddenly you don't want to discuss it anymore? Change the subject and run seems to be such a "stale" tactic.
"If there is evidence that HIV causes AIDS, there should be scientific documents which either singly or collectively demonstrate that fact, at least with a high probability. There is no such document."
Dr. Kary Mullis, Biochemist, 1993 Nobel Prize for Chemistry.
"Up to today there is actually no single scientifically really convincing evidence for the existence of HIV. Not even once such a retrovirus has been isolated and purified by the methods of classical virology." (Letter to Süddeutsche Zeitung 2000)
Dr. Heinz Ludwig Sänger, Emeritus Professor of Molecular Biology and Virology, Max-Planck-Institutes for Biochemy, München. Robert Koch Award 1978
" We can be exposed many times to HIV without having been infected and our immune system can get ride of the virus in a few weeks if you have a good immune system"
Luc Montagnier, House of Numbers Interview, 2006
"I do not regard the causal relationship between HIV and any disease as settled. I have seen considerable evidence that highly improper statistics concerning HIV and AIDS have been passed off as science, and that top members of the scientific establishment have carelessly, if not irresponsibly, joined the media in spreading misinformation about the nature of AIDS."
Dr. Serge Lang, Professor of Mathematics, Yale University
"The HIV-causes-AIDS dogma represents the grandest and perhaps the most morally destructive fraud that has ever been perpetrated on young men and women of the Western world."
Dr. Charles Thomas, former Professor of Biochemistry, Harvard and John Hopkins Universities
"The HIV hypothesis ranks with the 'bad air' theory for malaria and the 'bacterial infection' theory of beriberi and pellagra caused by nutritional deficiencies. It is a hoax that became a scam."
Dr. Bernard Forscher, former editor of the U.S. Proceeding of the National Academy of Sciences
I see denialists have changed the subject rather than have to answer questions that they know will betray the one-sidedness of the film. Typical.
""If there is evidence that HIV causes AIDS, there should be scientific documents which either singly or collectively demonstrate that fact, at least with a high probability. There is no such document. Dr. Kary Mullis, Biochemist, 1993 Nobel Prize for Chemistry."
On the plus side they have answered one part of question A (does the film cite Mullis). Now will they answer the second part. Does it also mention that he believes himself to have been abducted by aliens and visited by glow-in-the-dark raccoons? Afterall, a balanced film should mention if the authorities they cite are not...balanced, right?
"We can be exposed many times to HIV without having been infected and our immune system can get ride of the virus in a few weeks if you have a good immune system Luc Montagnier, House of Numbers Interview, 2006"
This has already been explained several times now.
Perhaps you can provide us with the complete context of the quote (if there even was a context rather than uninformed cherry-picking in this film)?
"Does it also mention that he believes himself to have been abducted by aliens and visited by glow-in-the-dark raccoons?
Afterall, a balanced film should mention if the authorities they cite are not...balanced, right?"
No, attacking the messenger is a task best left to idiots. Pathologising dissent would is Seth Kalichman's job.
Tara, I am sorry to say this but no one give a shit about the other things you write about.
"Pathologising dissent would is Seth Kalichman's job."
should read
"Pathologising dissent would be Seth Kalichman's job."
"No, attacking the messenger is a task best left to idiots. Pathologising dissent would is Seth Kalichman's job."
And pretending that a propensity for conspiratorial thinking and far-fetched delusions do not affect one's credibility is best left to the gullible.
If someone is so far out there mentally that they claim such things, one cannot help but wonder whether the same problem affects all other aspects of their thinking. It is not attacking the messenger so much as questioning whether they can be a credible witness. This is done in courts all the time.
If you were on a jury and a witness claimed he saw the defendant murder someone, then followed it up with a parade of glowing woodland creatures, how much credibility would you give to his testimony?
If you choose to follow people with such far fetched notions, Pat, that is your right but don't expect us to simply regard it as irrelevant.
Speaking of Seth, I will add that this is a stunning example of something he mentions in his book. In denialism (of any sort) pseudoscience propagates itself by gravitating to any source that agrees with what the denialist already believes. They choose to follow and accept the word of anyone that agrees with their preconceived notions regardless of the credibility or background of the person as long it supports their faith in their cause.
Alien abductee (Mullis)? No problem! Nessie "expert" (Bauer)? Sold! Cancer denialist (Crowe)? Hell they'll take them, too! They don't even need to be scientists at all! All that is needed is for them to support the denialist's cause.
Thank you Pat for this fantastic example.
"If you were on a jury and a witness claimed he saw the defendant murder someone, then followed it up with a parade of glowing woodland creatures, how much credibility would you give to his testimony?"
If the waitress claimed the glowing fuzzy creatures had something to do with the murder then I would be highly dismissive, sure. On the other hand if someone tried to discredit her testimony by recalling a distant episode of her tripping on LSD, then I wouldn't think her testimony is necessarily unbelievable. It is subtle but if one fails to see the difference one is prone to miss out on vital testimony.
"Alien abductee (Mullis)? No problem!"
of course it is no problem, he was tripping on LSD, what else would you expect?
"Nessie "expert" (Bauer)? Sold!"
No, not sold. Not sold at all but what may that have to do with HIV?
"Cancer denialist (Crowe)? Hell they'll take them, too!"
What makes you say that I would? Your bias towards me no doubt. BTW I have lost family to cancer, thank you very much.
Thank YOU for your fantastic example of Schubladendenken.
But the film appears to rely on these people as authorities on the matter. If they say that HIV doesn't exist then it must be so. The film cannot show the scientific evidence for the denialist claim, so they argue from authority. That authority is necessarily undermined but the fact that they are not authorities on HIV to begin with, and that they are prone to making other scientific unfounded statements.
Perfectly valid method when applied to polemics. Were there any scientific evidence however, you would be right. The messenger is then irrelevant, mostly. But there is none or it would have been mentioned by you or other denialists. 10 year old quotes taken out of context will not do.
"Cancer denialist (Crowe)? Hell they'll take them, too!"
"What makes you say that I would? Your bias towards me no doubt. BTW I have lost family to cancer, thank you very much."
Sascha pretty much covered the rest of the point pretty well so I'll address this. First I was speaking of denialists in general, not you specifically. Second, if you feel offended by this then congratulations, you now know how many of the families abd other loved ones of AIDS victims likely feel about your AIDS denialism. I'd like to hope this would give you something to think about but I'm not that naive.
"Perfectly valid method when applied to polemics. Were there any scientific evidence however, you would be right. The messenger is then irrelevant, mostly. But there is none or it would have been mentioned by you or other denialists."
why do you say it would be mentioned by ???me??? of all people
Also, can someone please, please tell me WHAT I am in denial of, preferably someone from some authority with a VALID psychological profile of ME and only ME? because it ain't AIDS my Schubladendenkender friends. As far as I can remember, I once challenged the grossly overblown "estimates" of AIDS in Africa and the UN came to my "rescue" from the cyber sisters here and admitted that the "estimates" were some 30% lower then initially thought. Of course we need to agree on what "grossly" means. Unfortunately that "rescue" didn't "cure" me from that shoebox I was stuffed in. Does that mean then that one is an asshole "denialist" until at least partially vindicated but remains an asshole "denialist" because everybody remembers having labelled me as such before and put me into that corresponding shoebox? Once an asshole always an asshole?
And while we are on the topic of authority, I believe (in accordance with this blog's emerging logic) that Kerry Mullis is THE authority on PCR then. He did invent and receive a Nobel whatever-that-means-nowadays prize, no? And THE authority on PCR says quite clearely that AIDS science is abusing its scientific usefullness. So why doesn't that stick with anyone here?
Oh, that's right: he sees glowing raccoons and little green ET's WHILE tripping on LSD!
So, according to THAT well-rehearsed in-house logic, Gallo too must also be a fraud, because once a fraud always a fraud, right? Or are we in denial of his fraud? Or better yet, How did he escape his shoe box?
"10 year old quotes taken out of context will not do."
What 10 year old quote are you on about???
You are fantastic Poodle. You say that you were talking about denialists in general and not me but then you move on to say...
..."your AIDS denialism".
What, but just WHAT makes you think I deny the existence of AIDS??????????????????????????????????????????????????????
I need you to think about that but I won't even bother with hope. Your Schubladendenken is pathologically entrenched.
"Oh, that's right: he sees glowing raccoons and little green ET's WHILE tripping on LSD!"
Where do you get the idea that he was on LSD when he supposedly saw this? Can you reference this? If I recall correctly he denied being on drugs the night this supposedly happened. His version of the story, as I recall, was something along the lines of him walking to the outhouse by his cabin and then seeing a glowing raccoon which spoke to him in English. From his own comments on the event, it is quite clear that he does not believe them to be drug-induced. I can find a reference for this if you would like.
"And while we are on the topic of authority, I believe (in accordance with this blog's emerging logic) that Kerry Mullis is THE authority on PCR then. He did invent and receive a Nobel whatever-that-means-nowadays prize, no? And THE authority on PCR says quite clearely that AIDS science is abusing its scientific usefullness. So why doesn't that stick with anyone here?"
First off, I believe (although I could be wrong)that Mullis disputes the use of PCR to quantify HIV, not simply detect it.
He has been quoted as saying that:
"PCR made it easier to see that certain people are infected with HIV.
indicating that he has no doubts that HIV exists and can be detected by PCR. What he disputes is that HIV is the cause of AIDS.
However, quantitative PCR is different from the PCR "invented" by Mullis. Real Time Reverse Transcription PCR is likewise different from the very basic version of PCR that Mullis "invented". As such, he is no more an authority on these subjects than the man who invented the wheel is an authority on whether or not a Cadillac is possible.
Secondly, Mullis did not so much âinventâ PCR (although he is generally credited for it) as made it available in a widely available and convenient form. The earliest reference to a PCR-like reaction was in 1971 by Kleppe et. al, 12 years before Mullis' PCR. Like Mullis, they are not automatically considered THE authorities on all variants of PCR simply because they came up with an early version of it.
âWhat, but just WHAT makes you think I deny the existence of AIDS?â
Iâm sure you have your own definition of AIDS which you do not dispute, however you seem hell bent on denying any and all evidence that HIV is the cause, instead gravitating towards very questionable authorities with no expertise on the subject in order to deny that HIV is the cause or exists (I forget which one you are). If I am incorrect on this then by all means say so, I donât profess to be always right. This type of denialism is similar to other types including holocaust denialism, moon landing hoaxers, flat earthers, and IDers. The basic pattern is as such:
1) Misquote studies (take the oft-misquoted Padien study, for example)
2) Spurn actual experts in the field, citing conspiracy by some omnipotent force like big pharma, the government, aliens, you name it.
3) Cite non credible fringe authorities and anyone else that supports the cause.
4) Claim censorship by intimidation/firing of those who speak âthe truthâ about the issue
Well you get the picture.
Whenever one of the quacks comes on denying AIDS even exists, you come out arguing against any who do not agree with them. It is true that you do not actually say AIDS doesn't exist, but all you are doing is fence sitting. Maybe you should clarify your actual position concerning AIDS, so we may avoid mistaking you for what you are not.
Estimates are just that, estimates. They are subject to review and may may vary greatly. I still fail to see what your problem is concerning the UN numbers?
I didn't say that arguing from authority is a valid method, I said that disputing the credibility of the those who do is perfectly acceptable. Also, again I notice you only ever cite those that deny AIDS exists.
The quotes are those that were being discussed earlier, those from the authorities used to buttress the claim in the documentary. You came out defending the credibility of these "witnesses".
But Sascha, if he actually states a position he would be obliged to provide evidence to support it and he would also be obliged to stick to the position and not swap between mutually exclusive arguments.
The beauty of denialism is that you can avoid this by just criticisng others. Just watch from the sidelines and take potshots.
One of the paradoxical things about HIV/AIDS denialism is how ready denialists are to make arguments from authority while at the same time claiming an anti-authoritarian stance.
There are two ways denialists and other pseudoscientists such as creationists try to get away with this.
The first is to only cite âauthoritiesâ who arenât in fact experts in the fields theyâre shooting their mouths off about - like Mullis, Sänger, Forscher, etc.
The alternative is to quote-mine genuine authorities or even ordinary everyday scientists making factual reports, making sure to edit out any hint of context that would alert a reader of average intelligence that the speakerâs words are being twisted or misrepresented to make them seem like they are saying the exact opposite of what they are trying to communicate â like Montagnier.
Some denialist websites excel at both these forms of dishonest rhetoric. Combining two or more different types of deception can make it easier to overcome resistance to deceit. Itâs David Croweâs (for example) favorite way of lying. The strategy is also commonly used by propaganda films â the type species here is Ben Steinâs Expelled â No Intelligence Allowed and it looks like we have a similar specimen in the pseudoscience genus here in House of Numbers.
W00t!
"however you seem hell bent on denying any and all evidence that HIV is the cause, instead gravitating towards very questionable authorities with no expertise on the subject in order to deny that HIV is the cause or exists (I forget which one you are)."
So in other words:
when in doubt just call them AIDS denialists. It sticks like crazy glue.
In the case of Maggiore I am merely defending her right and obligation to make health descisions for herself and her family (whether or not she made the right decision) because no one else can or is willing to take on that responsibility themselves. The best anyone can do really is "...watch from the sidelines and take potshots". It is an art form here. I am also simply trying to correct those who are hell bent on misquoting her such as her telling people "to have unprotected sex" or that she actively seeks to get people off the meds.
From her Memorial wall:
"I learned of Christine's death at 3AM on Monday morning when a mutual friend emailed me. For whatever reason, the vibration of my iPhone woke me up.
It seemed like a bad dream that I couldn't wake up from. I have been HIV+ since 2000 and met Christine in that first year. I didn't expect to like her, but I was writing an article about AIDS Dissidents and she was on my list of people to interview. What surprised me most about her was that she was so unassuming. She never yelled or talked down. In spite of her strongly held and controversial beliefs, she never stood on a soap box, never preached and always respected the views of othersâeven when they were not showing her the same deference.
Later that year, I was in LA and Christine and Robin allowed me to stay at their home and that was the beginning of a a great friendship. She and Robin were like family and I came to think of EJ and Charlie as a niece and nephew. My views on HIV differed from Christine's in that I believe there is a retrovirus and that in some people, that virus negatively impacts the immune system. Where we found much agreement was in the toxicity of the drugs. Yet in spite of this difference, Christine never tried to convert me or change my point of view and in doing this, she empowered me to make my own choices, to think critically and to take responsibility for my own health.
In 2006, I made the very difficult decision to go on meds. Ironically, it was Christine who supported me the most. This is not to say that she agreed with the decision, but she sat with me while I cried and weighed the pros and cons. Not once did she try to force her personal views and choices on me. Honestly, I was fearful that my decision to take meds would impact my friendship with her, but in truth, that decision seemed to bring us closer together.
I don't know what I will do without her in my life. I suppose, her greatest lesson is that, in spite of grief, hardship and adversity, we are all capable of thinking for ourselves, making choices even when they are not easy and in doing so, fully embrace life. Sadly many people think that Christine's work was about HIV, but really it was about empowering people and that is what made her such a force for healing in this world.
Christine will be vilified by some and celebrated by others. For me, however, she will be held in my heart with tender love and eternal gratitude. I am 'alive and well' today because of Christine. Not simply because of her workâ but because of who she is, how she lived and the hand of friendship she so selflessly extended to me. What is even more heart warming is that I am not alone. I know that Christine had this effect on thousands of people around the world and now each of us, in our own unique way, can share what she taught us about life. There is a saying, "Only God knows how many apples are in an apple seed." As she walked her path with the heavy burdens life had bundled on her back, she continually planted seeds of hope, compassion and informed decision-making. The question now, is how many of us will allow those seeds to grow in the lives of the people that cross our path. I can think of no better way to honor Christine than by planting the seeds.
Darren Main
http://www.darrenmain.com"
Oooops, didn't see that one coming!
So I find it strange that defending this obvious right and obligation of hers makes me deny the existence of AIDS. I'll try to wrap that one around my head but don't hold your breath.
"I donât profess to be always right."
No shit.
"I didn't say that arguing from authority is a valid method"
You didn't?
"That authority is necessarily undermined but the fact that they are not authorities on HIV to begin with"
I thought HIV was a retrovirus so by default Duesberg would be "an" authority on it, no?
Let me see where this exchange will lead us...
-No,no,no! He has never studied HIV!
-didn't he try several times to get grants to study it?
-Yes, but he was denied all any any grants to get anywhere near HIV.
- why is that?
-Because he is a crack pot and denies HIV causes AIDS! If he wants to study it he should simply inject himself with it and see the results! He also has friends that see glow in the dark raccoons and Nessies and they are all Germans anyway! (that last bit is part of Seth's pathology of dissent FYI)
Aaaah, the science of blogging; advancing one flame job at a time.
It is one o'clock, I am off to have a life now. I'll check in later.
Hi chris N, bye chris N.
"I thought HIV was a retrovirus so by default Duesberg would be "an" authority on it, no?...Let me see where this exchange will lead us..-No,no,no! He has never studied HIV!-didn't he try several times to get grants to study it?-Yes, but he was denied all any any grants to get anywhere near HIV.- why is that?"
Try this: Duesberg did his work with simple retroviruses and applied what he observed there directly to HIV with no experimental evidence to back him up. The problem of course is that HIV is NOT a simple retrovirus. HIV is a complex retrovirus, specifically a lentivirus and he knew this as it was established very early on. The difference is that HIV has a host of accessory genes that Duesberg had never studied. Thus, for him to apply everything he thought about simple retroviruses to HIV was incorrect. It is like comparing a bicycle to a corvette and claiming that in accordance with the comparison, the corvette should not be able to go fast. He would have been much better off comparing it to other lentiviruses which share many characteristics with HIV.
Now mind you, his comparison would not have been scientifically invalid if he were open to evidence counter to his claim. However, even when studies showed that drugs did not cause AIDS, he stuck to his same original story with no support for it. That is bad science. That is why mainstream scientists no not view Duesberg as an authority on HIV.
"no not view" should have been "do not view"
Pardon my french. I was making a comment on your chosen authorities. To argue that something is so because someone in authority has said so, is arguing from authority. In this case the authority can be as much Crowe as Gallo, or Mickey Mouse for that matter.
To argue that to be credible, one needs a certain knowledge if not authority on the matter is not arguing from authority. It is simply presuming one has a certain knowledge of the matter before starts making claims about it. it goes to that person's credibility.
Duesberg is not an authority on HIV so his credibility can and was questioned. When Duesberg claimed that the scientific consensus was wrong about HIV, the fact that he was- and remains to this day - not a specialist on HIV will cause those that are specialists to be "skeptical" (lordy me, I said it.) of his claim. They wanted to see evidence that backed him in his statement. 25 years later the world still waits.
By the way, the great Galileo Galilei once affirmed that the solar system was solar centric and was later proved to be right. He was in fact an authority on the solar system, spent more hours observing the heavens then any before him - i believe even more than Tycho Brahe. He developed the first astronomical telescopes to better observe the movements of the stars, and yet he still got his theory of the tides wrong. You again are confusing being an authority on something and being right about something.
If you want to claim that a world wide conspiracy is undermining his every attempt to affect research on HIV, then please provide some evidence for that.
You get your pantyhose all wrapped up about Maggiore's HIV status, claiming everybody here - with the exception of the wackos, nota bene - is grave dancing and carries as much responsibility for Maggiore's death as she herself. That is patently absurd. She was an adult who made her choices and had to live with them.
Normally these choices would be nobody else's business but hers. She chose to make them public and use her status to push her agenda. She made discussion of her status relevant and fair game. I am having a hard time understanding why you are so touchy about this. As for responsibility she alone carries the responsibility for her death. She made that choice.
The problem is greater when you consider the health of the children she is responsible for. The child cannot make the informed decision you claim Maggiore was entitled to make. The child has an interest in the matter that is seperate from the parent's interest, it may even enter into conflict with the parent's own interest.. That is where the authorities come in. If a parent refuses to allow her child to be treated according to the accepted practices of medical science than the state has a responsibility, de lege, to investigate and insure that parent has good and valid reasons to refuse the treatment. Determining beforehand what risks that child may be exposed to is part of the process. that may even include determining one's HIV status. As far as I know the state looked into the matter and found no reason's to intervene. Maggiore was allowed to make all of her children's relevant medical decisions by herself. I fail to see the incredible abuse of process you allude to. As for blogger's opinion's concerning her decisions, the moment she made her stance public and part of her agenda then she and her decisions become fair game.
You can disagree about the need for the state to intervene in a parent's decisions concerning her child's welfare. But that is something you must take up in your local house of representatives. Awaken your civic responsibility and change things. Do it.
No I'm off to get a life. I'm pushing to get the gardener to admit that the orthodox meme that claims plants actually grow is wrong and costing me a fortune. Everything I plant dies. It's a big con by Big Gardening firms trying to sell me their overpriced automated watering systems.
P.
Passed mémoire with 6!
S.
If you have any information about any of Duesberg's grant applications then please fill us in.
I don't think he ever made any that involved HIV. He did send in some that involved giving poppers to mice but they were rejected on scientific grounds that had nothing to do with any alleged political conspiracy.
If you do have any details about his grant applications then by all means post them.
Why doesn't Duesberg publish his grant applications and the reviewer's comments?
Iâm not sure itâs that clear cut. Maggiore did not act alone.
While the decision to thrust herself into the spotlight was ultimately her own, she wasnât the only one who put her there. There were a lot of people who had an investment in her continuing to reject mainstream health care, and her somewhat garbled public pronouncements on HIV/AIDS. She became their poster girl, and to some extent their pawn. Denialism became a trap so horrible I would not wish it on anyone, but Maggioreâs personal tragedy was scripted by multiple writers, not just herself. After she died they have been trying to rewrite her as some kind of martyr-hero. I find that nauseating.
I have no trouble at all understanding why denialists get touchy about this.
As mentioned on Seth's Blog, there is another Tennessean entry related to the House of Numbers movie. The link can be found here.
The director was previously making a film based on the Boyd Graves conspiracy theory of HIV creation.
Are we supposed to believe that Brent Leung does not have an agenda?
Snout,
Of course many more people were involved, but the decision was hers alone. Barring proof to the contrary she made an informed decision concerning her own health care. You may disagree with her decision but I for one will defend her right to make it. Even if we all know it was a mistake.
I too can understand why denialists are touchy, but my question was to pat who claims not to be a denialist. Or at least implies it.
"In the old days it was required that a scientist address the possibilities of proving his hypothesis wrong as well as right. Now there's none of that in standard HIV-AIDS program with all its billions of dollars."
Dr. Richard Strohman, Emeritus Professor of Cell Biology at the University of California at Berkeley
"Unfortunately, the AIDS 'establishment' has formed that intends to discourage challenges to the dogma on one side and often insists on following discredited ideas on the other."
Dr. Roger Cunningham, Immunologist, Microbiologist and Director of the Centre for Immunology at the State University of New York at Buffalo
"Dominated by the media, by special pressure groups and by the interests of several pharmaceutical companies, the AIDS establishment efforts to control the disease lost contact with open-minded, peer-reviewed medical science since the unproven HIV/AIDS hypothesis received 100% of the research funds while all other hypotheses were ignored."
Dr. Etienne de Harven, Emeritus Professor of Pathology, at the University of Toronto
"In defending the purchased consensus, HIV researchers use statistical methodologies shown by their inventors to be invalid and conduct experiments without any controls. They take causes for effects, correlations for causations, and constants for variables. Most important, they havenât stopped AIDS. What they have done successfully is instilled fear into human sexual relations -- an amorphous fear, which most AIDS professionals as well as journalists argue has been valuable."
Dr. Dave Rasnick, Biochemist, visiting scientist University of California at Berkeley.
Quotes and more quotes! But where's the beef?
Arguing from authority again. They say so , so it must be so. A new religion is born. I deny all therefore I am.
Why am I so skeptical, why must I question everything. Why must I deny denialism? Does that make me a dedenialist?
To the troll (Denialist @ UCB, VIRUSMYTH DOT COM, SUNYB, Yales best, H-I-what???, Harvard Boyz, etc):
Yes we all congratulate you on discovering how to copy-paste drivel from Virusmyth. We are all well aware that what passes for "intelligent" argument from AIDS denialists basically boils down to:
Ctrl+X,
Ctrl+V,
Repeat.
Thanks for demonstrating it.
Now kindly fuck off â you are as cogent and welcome as the Turkish malware spam that commonly infests the tail end of these Aetiology threads (and no, Iâm not referring to Sadun Kal).
Please run along back to AIDS Myth Exposed where you usually like to hang out.
The grown-ups are trying to have a conversation here.
Sascha, I think there is a moral and political issue of accountability here.
If a medical doctor gave Maggiore advice based on his or her own personal egotistical hobby horse beliefs rather than real science, that Maggiore relied on and as a result her child died, and then she herself died, then the doctor would be held accountable. Morally, and legally â possibly criminally.
People have a right to make health decisions based on informed consent. The principle of informed consent is not carte blanche for every nutcase on the planet to demand a hearing for their misinformation.
The fact that Maggiore was a legally competent adult in no way expunges that responsibility on the part of her advisers to take reasonable care in the advice they give, and they should be accountable for the consequences of that advice.
Along come cranks, quacks and sociopaths like Duesberg, Bauer, Rasnick, Crowe, Rath and the rest of the denialist pantheon with their own agendas. They abuse the power structures of society and a bogus appeal to âfreedom of speechâ to override legitimate medical authority.
For all its systemic failings, medical authority derives its legitimacy not just because doctors (and other legitimate health professionals like nurses, physiotherapists, etc) are properly trained and experienced and answerable to the laws of the land, and certainly not because they make a moral claim to altruism or to know best, but because they can be held accountable for their actions.
In a democracy, legitimate health professionals are answerable not only to their patients directly, and to the coursts, but also to their regulatory boards. The regulatory boards are answerable to the relevant health departments, the health departments are answerable to the elected government, and the goverment is answerable through elections and through media scrutiny to the people. Thatâs what liberal democracy is: itâs a system of accountability where ultimate authority lies - the buck stops - with the people.
The agenda of AIDS denialist cranks seeks to override that system of accountability. Like narcissistic children they demand to be listened to, but accept no responsibility at all for the consequences of their actions. And in doing so they seek to undermine the legitimate systems of accountability that are foundational to liberal democracy.
Thatâs what makes me fume. They should not get away scot-free.
Couldn't agree more. If a medical, or any other professional for that matter, misinforms a patient, than he should be, and mostly will be, held accountable.
In the Case of Maggiore, I'm wondering if the misinformation could be considered determinant (is that the right word?) of her consent. What I mean by that, is that Maggiore went to great lengths to inform herself and was necessarily aware of the highly controversial aspect of the information she was relying on. I imagine It would be very difficult to sustain the position that she was mislead by a professional to such a degree that her consent could not be considered informed.
That the practitioner remains responsible, criminally, civilly and administratively, is in no doubt. But she was not some blue-eyed naive civilian who had absolutely no idea that her practitioner was misleading or misinforming her. She bears the responsibility for her choices.
I completely agree with Snout. He said: "The goverment is answerable through elections and through media scrutiny to the people. Thatâs what liberal democracy is: itâs a system of accountability where ultimate authority lies - the buck stops - with the people."
Snout, you are right on Target. Science should certainly not be decided by scientists but by the people who pay them. What is scientifically true or false should ONLY and EVER be decided by the media and by popular public vote.
And now that Snout and I both have officially voted for HIV to be the cause of AIDS, we need to figure out how to control the pesky media from ever mentioning the damned aids denialists as having any credibility. The people need to control this issue, not science, and not government and not media.
Down with AIDS doubters, and Down with any media that backs them. Up with People. Up with HIV. Up with AIDS. And three cheers for HIV causing AIDS! Long Live HIV! GO hiv Go!
The people have spoken! Right Snout?
You haven't understood a word Snout wrote, have you.
Go back over it, read it again, breath in deeply and read it another time. Get out your dictionary to look up those words you don't understand. Think, it's a very important part of reading. Read every word and place it in it's context, find the subjects, the verbs and the adjectives; determine which modifies what.
If you still come to the same result as your previous inane post, try again. Never give up; it might take longer than for others, but you'll eventually get there.
Shut up Sascha.
The people have spoken. Right Snout?
Hiv IS the cause of aids. Go hiv. Go Aids.
Sascha. You are either with the people on this or against us. What's it gonna be?
Long live hiv/aids!
Snout,
Correct me if I'm wrong, but wasn't Maggiore's family doctor disciplined by the local regulatory board?
Don't give up, try harder. You will eventually learn to understand what you read.
If the only thing holding Democritus and these other "enemies of faith" back from total and complete assimilation into atheism was general ignorance about earthquakes and weather patterns, then 1, why are you assuming that they would NOT arrive at the same conclusion as today's atheists if handed a science textbook, and 2, since they were critical of the beliefs of their time, then they ought to be distinguished for their lumpen behavior not generalized as simple theists.
"Cancer denialist (Crowe)? Hell they'll take them, too!"
"What makes you say that I would? Your bias towards me no doubt. BTW I have lost family to cancer, thank you very much."
Sascha pretty much covered the rest of the point pretty well so I'll address this. First I was speaking of denialists in general, not you specifically. Second, if you feel offended by this then congratulations, you now know how many of the families abd other loved ones of AIDS victims likely feel about your AIDS denialism. I'd like to hope this would give you something to think about but I'm not that naive.
Looks like the Turkish trolls have taken to copy-pasting old posts to make themselves harder to spot...
Sascha, I don't know a lot about Maggiore's family doctors, but there's an article on Paul Fleiss here:
articlesDOTlatimesDOTcom/2007/oct/09/local/me-fleiss9
(I always seem to get stuck in Tara's spam filter when I try to post links)
and AIDS Truth has something on Ilona Abraham, who looked after Maggiore during her final illness.
wwwDOTaidstruthDOTorg/new/news/2009/christine-maggiore-died-aids
Hey Snout,
Did you know that Dr. Charles Thomas, Molecular Biologist and former Harvard and Johns Hopkins Professor, said:
"AIDS has been a disease of definition. If we said that it didn't exist and didn't pay for it with taxpayers' money, it would disappear in the background of normal mortality."
Off with his head! The people have spoken. Long live hiv/aids. Right Snout?
And that damn Dr. Mohammad Ali Al-Bayati, Toxicologist and Pathologist, said:
"HIV does not cause AIDS. There is no scientific evidence that HIV can kill infected T4 cells. The true problem is that the leaders of the HIV hypothesis have been ignoring important medical facts and are blindly attributing AIDS to the HIV virus. It is very sad and frustrating to know that the AIDS establishment are giving highly toxic drugs such as AZT to pregnant women even with studies that show the depression in the immune system can be reversed by nutrition. Prescribing anti-viral drugs to AIDS patients is like putting gasoline on a fire"
Off with his head too, cause me and snout and seth kalicksman, and chris and poodle are the nonscientific spokespersons for hiv and the people, and we the people could not care less if there is no evidence that hiv kills T cells, cause WE SAY hiv kills t cells and WE SAY it causes aids.
Long live t cell killing hiv and aids! Down with science and scientists. Power to the people! Right Snout?
"While first learning about the AIDS controversy, I read whatever I could on both sides. I have not found an instance, when both sides have been able to state their complete case, where the mainstream AIDS view has held up. On the contrary, much of the mainstream view seems to be based on bad research and fallacious reasoning."
Dr. Rush Wayne, M.A., Molecular Biology, Harvard University, PhD, Biochemistry, University of California
--------------------------------------------------------------
Well, who cares what some molecular biologist from Harvard says!
We the people have made our choice. Hiv kills t cells and causes aids cause we say so.
Right Snout?
I agree with Snout! All those doctors and scientists that say hiv / aids theory is bullshit must be banned from speaking, and the only ones who should be allowed to speak are the ones who say what we the people want to hear. Cause just like Snout says:
"Thatâs what liberal democracy is: itâs a system of accountability where ultimate authority lies - the buck stops - with the people. They (scientists and doctors who disagree with popular public opinions) seek to undermine the legitimate systems of accountability that are foundational to liberal democracy. Thatâs what makes me fume. They should not get away scot-free".
I completely agree with Snout. Makes me fume too. How dare they disagree with the people! Scientists don't mean nuthin! And unless they agree with us, they should only be seen and not ever heard from! If they speak out, then Hang em high and start with Duesberg!
Up with people, and down with scientists speaking their mind! Long live hiv causing aids. The people have spoken! The dissidents are outnumbered so that means We rule!
Right Snout?
Snout,
I believe it was Fleiss I had in mind, thanks for the links.
No worries, Sascha.
"A kind of collective insanity over HIV and AIDS has gripped leaders of the scientific and medical profession. They have stopped behaving as scientists, and instead are working as propagandists, trying desperately to keep alive a failed theory."
Neville Hodgkinson, former Science Editor, The Times of London:
You know, spamming cherry picked lines and quotes from people barely qualified to tie their own shoes works just about as well as standing on a street corner yelling "Convert or suffer the consequences you sinners!"
On the other hand it gives valuable insight into what kind of authorities denialists trust.
If the Thunderer says so then, it must be true.
Heraclides,
Putting a stupid grin after every paragraph does not constitute good writing or civil communication (-; It's just childish doodling (-; Try a creative writing class and come back in a few years (-;
In the meantime, if one has to try to decipher "sentences" like this:
"Have fun, don't get too wound up! ;-)"
I'd say advising people not to get wound up followed by an idiotic doodly thingie is pretty darned close to laughing and telling people to calm down (-;
I'm waiting for an apology, not only for sliming my screen, but also for avoiding the substantive issue (-;
Very Sincerely Yours
)-;... Nah just kiddin', take it easy (-;
Thanks You.
have not found an instance, when both sides have been able to state their
I'm waiting for an apology, not only for sliming my screen, but also for avoiding the substantive issue (-;
when both sides have been able to state their
Very late, but just found out that an article about Tommy Morrison that was referenced around comments 280-295 was reprinted in 2008. The original printing was in 1998, which clarifies a number of discrepancies. Just wanted to set the record straight.
I'm waiting for an apology, not only for sliming my screen, but also for avoiding the substantive issue.