HIV Test bogus, says PCR inventor

Great Debates
301

trueskeptic
From the little I’ve read about SMON, it was is nothing as huge as you make it seem. It was first noted in the 1950s in Japan in a few cases. It was named in 1964, and by 1970, pathogenesis by clinoquinol toxicity was well nailed down. Before then, a few scientists proposed a viral nature, but it was strictly a guess. It was not the huge wrong commited by the entire medical community that you make it out to be. It was a tiny outbreak in a small community without access to current technology and diagnostic techniques. This kind of reads like the creationists’ cries about Piltdown Man. They claim it was a huge fraud which the evolutionists bought en masse, and was decades before it was disproven. In fact, it was only bought by a few people, it was never subjected to rigorous testing and the best techniques available, it was not repeated, and was quickly discredited.

We are not talking about a presumptive hypothesis floated as the cause of a small outbreak in a small medical community. We are talking about a worldwide conspiracy to suppress evidence in a global pandemic that has so far killed millions. Slightly different, I hope you will agree.

Next, gastric ulcers. If you are asking for an answer for when the exact paradigm shift happened in the Marshall case, I think that question is unanswerable. Scientists and doctors are just people – some will keep disproven beliefs long after good science shows them wrong. Not everybody reads the literature in great detail and modifies their medical and scientific practice immediately. There is no organized opinion-making body in science that tells everybody what to believe.

But, I’ll hazard that few people found much reason to “ridicule” Marshall (and I still haven’t seen a cite of this ridicule – one guy calling the theory preposterous doesn’t really count, especially since that guy quickly was convinced of H. pylori) after the Lancet article. Or after that one was confirmed.

Now, to primary data that would uphold your hypothesis. This is a good line of conversation. I will define AIDS as an acquired CD4+ T-lymphocytopenia that leads to opportunistic infections (OIs). The exact nature of the OIs are determined by a whole host of factors.

What we are concerned about is not the OIs, which have variable clinical presentation. We are concerned about AIDS. My side argues that the cause of AIDS is HIV; yours argues that it is sexual promiscuity, drug use, and antiretrovirals.

So, your side needs to explain some things:

  1. How do sexual promiscuity, drug use, and antiretrovirals cause a specific decline in CD4+ T-cells? Are there molecular mechanisms?
  2. Can you make a dose/response correlation between CD4+ T-lymphocytopenias and exposure to sexual promiscuity, drug use, and antiretrovirals?
  3. Are there cases of acquired CD4+ T-lymphocytopenias that occur in HIV- individuals? Are these explained by sexual promiscuity, drug use, and anti-retrovirals?
  4. How do you explain AIDS cases in patients with no documented exposure to any of your risk factors, namely health care workers and transfusion recipients who have contracted AIDS?
  5. How does HAART, or highly-active anti-retroviral therapy, a treatment specifically targeted against enzymes only found in HIV reverse a CD4+ T-lymphocytopenia caused by sexual promiscuity, drug use, or anti-retrovirals?
  6. Do your risk factors explain the clinical course of AIDS better than the HIV theories?
  7. Do your risk factors explain the laboratory findings of AIDS better than the HIV theories?
  8. Does abatement of your risk factors lessen or reverse the disease? What is the molecular mechanism of “lifetime accumulation” of these toxins and other baddies? Are there clinical measures available for assaying “lifetime accumulation?”

This is just a small list. The biggest hole I can see in the argument is with #3 and idiopathic CD4+ T-lymphocytopenia (ICTL), which is an incredibly small sliver of people with a markedly different presentation than AIDS. But drug use, promiscuity, and antiretrovirals doesn’t explain ICTL any better than HIV. It is a zebra, and an exception, which is totally not unusual in medicine.

Look at it simply, with relation to gastric ulcers and Marshall. Q1: What was the old theory? A: gastric ulcers are caused by stress, NSAIDs, or unexplained factors leading to too much acid or mucosal erosion). Q2: Does the theory do a good job at explaining ulcers? A: Not really because while we can treat the acid, we don’t know what the root cause of the acid is. Q3: Is there a new hypothesis? A: Marshall proposed H. pylori. Q4: Does it explain it better than the old theory? A: Absolutely – introduction of the bacteria leads to disease, treating the bacteria treats the disease. It explains most cases of ulcers and gives us mechanisms of this unknown mucosal erosion.

So, we know the old theory. We know the new hypothesis. Does your stuff explain stuff better than the old stuff? Does it give us better understanding of the disease? Does it give us new insights into treating the disease? The answer seems to be no on all counts. Unless you can show me literature which suggests differently, I will be steadfastly unconvinved, as would any scientist.

302

I’m still trying to figure out how all those heterosexuals in Africa got infected with HIV and developed AIDS. Was that part of their habitual drug use and partying lifestyle? Heck, I didn’t even know you could get poppers in the third world!

:rolleyes:

Esprix

303

Esprix,
Don’t cha know? It is the plutonium in the vaccines that is causing African AIDS!! (from aliengraves cite – http://www.whale.to/a/lanka.html)

In actuality, they somehow claim that African AIDS, another acquired CD4+ T-lymphocytopenia leading to characteristic opportunistic infections that is tightly linked to an infection with an HIV retrovirus, is a totally different disease than our AIDS. Not that they try to explain the differences, not that they give us an explanation of African AIDS, etc.

As soon as you force these type of contrarians to debate the science, their arguments fall apart like wet tissues. Young earth creationists and HIV deniers are just the easiest of the lot.

304

The science involved with parsing out the precise interlocking mechanisms of the HIV>AIDS infection model is extraordinarily complex as is the HIV virus itself. I am not a research scientist, nor do I have anything more than a layman’s understanding of the complexities of HIV virology. It is also evident that your grasp of current HIV virology, techniques and research is somewhat tenuous as well, as is evident by the fact that edwino’s quite specific questions to you are going largely unanswered, and your only response is to disgorge another cut and paste-beside the point glurge from a 10 year old study or something of similar scientific weight.

So, like the hedgehog I may only know a few things, but I do know this -

There are billions of dollars being invested worldwide in a desperate search for a solution to the ravages of AIDS through science being conducted by some of the most powerful scientific intellects of our generation. The HIV>AIDS viral infection model has been established as a near certainty, and this working hypothesis is confirmed and re-confirmed again and again in therapies that seek to break the HIV replication process, and have been effective in stopping the symptoms of the AIDS disease in its tracks if started early enough, though not eradicating it from all it’s hiding spots in the body.

The therapies to date are complex, physically enervating and quite expensive. There are powerful and interested parties in the form of insurance companies and governments etc. that would love to see a less expensive and more permanent solution than the current complex and expensive anti-viral therapies. The “system” is this case would love an alternative model to the HIV>AIDS hypothesis.

Unlike the wonderful examples of the research discussed in this thread conducted by Prusiner and Marshall that generated hard, paradigm changing data, the HIV>AIDS contrarians have an empty basket of old, largely irrelevant research and must rely on Johnny Cochran like rhetorical dances and hand waving to dispute the flood tide of data currently being generated that supports the HIV>AIDS hypothesis. The HIV>AIDS contrarians attribute the lack of support for research into alternative AIDS disease models to a near conspiracy by a confederacy of corporate, medical, scientific and governmental dunces who will not open their eyes to the fact that AIDS could be caused by drug abuse, anal sex or as the rappers say ‘hard livin’.

Real research scientists doing real research and getting real results look at these contrarian claims and the data they are predicated on. The contrarian data is old (antique, in fact, by current AIDS research standards) and essentially irrelevant, because it is contradicted by the more recent data using newer and more powerful research tools. Out of the thousands and thousands of research scientists currently doing AIDS research, and doing new research that is currently being published, there is not a single, solitary one willing to buy into the contrarian model. This, from a group of highly intelligent, highly trained professional skeptics, and, in many cases, highly competitive people, who would love to get a leg up on the problem and receive the laurels for finding a solution.

Now, from my layman’s perspective I could attribute this to the fact that these researchers are blind fools, and that there is a diabolical conspiracy between various governments and insurance companies to waste as much of their finite financial resources as possible… or I could attribute this to the fact that the contrarians are simply not bringing much to the table or they would not be flogging old research that has long been passed by, and absolutely bizarre arguments about the human bodies potential auto-immune reaction to anal sex and amyl nitrate (poppers).

The bottom line trueskeptic is that you guys are not bringing much to the table to support your arguments in a coherent fashion, other than rhetorical contortions to try and explain away the powerful results of the current HIV>AIDS paradigm, and the poorly supported contrarian assumption that current AIDS research is beside the point because it is founded on faulty epidemiological premises. Assumedly contrarians as a group are not a gaggle of impoverished bumpkins. Collect some funds then put your money where your convictions are, do some research and then come back when you’ve got more to debate with than a hatful of nonsense.

305

See? Seven pages. I told you we could have a debate about this.

I think the HIV orthodoxy has won so far, but shouldn’t Cecil have an article about this to help stop ignorance?

306

Edwino writes:
“As soon as you force these type of contrarians to debate the science, their arguments fall apart like wet tissues. Young earth creationists and HIV deniers are just the easiest of the lot.”

I encourage everyone to go back and read my debate with Edwino in this thread over a paper he presented as evidence HIV causes AIDS. You will see that he didn’t even understand the basic definitions the researchers used in the paper. And he is the one who cited the paper! Edwino is the one who doesn’t have the ability to debate (or even understand) science!

Astro writes:
“There are billions of dollars being invested worldwide in a desperate search for a solution to the ravages of AIDS through science being conducted by some of the most powerful scientific intellects of our generation. The HIV>AIDS viral infection model has been established as a near certainty, and this working hypothesis is confirmed and re-confirmed again and again in therapies that seek to break the HIV replication process, and have been effective in stopping the symptoms of the AIDS disease in its tracks if started early enough, though not eradicating it from all it’s hiding spots in the body…
Real research scientists doing real research and getting real results look at these contrarian claims and the data they are predicated on. The contrarian data is old (antique, in fact, by current AIDS research standards) and essentially irrelevant, because it is contradicted by the more recent data using newer and more powerful research tools. Out of the thousands and thousands of research scientists currently doing AIDS research, and doing new research that is currently being published, there is not a single, solitary one willing to buy into the contrarian model. This, from a group of highly intelligent, highly trained professional skeptics, and, in many cases, highly competitive people, who would love to get a leg up on the problem and receive the laurels for finding a solution.”

If it were true that the HIV>AIDS hypothesis has been confirmed again and again, then why would the following petition by scientists be necessary? Note that Nobel prize winners and science professors from top research universities signed the petition:
http://www.virusmyth.net/aids/group.htm
"It is widely believed by the general public that a retrovirus called HIV causes the group diseases called AIDS. Many biochemical scientists now question this hypothesis. We propose that a thorough reappraisal of the existing evidence for and against this hypothesis be conducted by a suitable independent group. We further propose that critical epidemiological studies be devised and undertaken. "
Here is a descrition of the petition group http://www.virusmyth.net/aids/data/drblinded.htm
"The Group for the Scientific Reappraisal of the HIV Hypothesis was founded by former Harvard professor Charles Thomas in 1991. Today more than 500 scientists, health-care workers, and other professionals have signed on.

What distinguishes this group? By and large, its members are not dependent on grants from the National Institutes of Health for their livelihood. The signatories who are Nobel laureates are immune from bureaucratic intimidation. Many of the academic members of the group who publicly support Duesberg are emeritus professors, whose careers can’t be terminated. Younger academics, on the other hand, who have seen the establishment mercilessly punish and excommunicate someone of Duesberg’s stature have clearly gotten the message: They keep their mouths shut and bow down before the golden calf of HIV.

Serge Lang, the legendary Yale mathematician and member of the National Academy of Sciences, has had so many letters to editors concerning the HIV scandal refused publication that he started sending checks along with his letters - the equivalent of buying space in which to speak. (Some editors were sufficiently embarrassed by this tactic that they published Lang’s letters and returned his checks.)"

Astro writes:
“I am not a research scientist, nor do I have anything more than a layman’s understanding of the complexities of HIV virology.”
Thank you for your admission. I think you owe the research scientists above an apology for your written abuse.

307

Hmmm… a ten to twelve year old list. Fascinating! Out of purest curiosity I wonder two things about this decade old list you have linked to-

1: How many of the people signing this list in the early 90’s when much less was know about the disease than is known today, would be willing to sign it now given the far more comprehensive understanding we have about the viral mechanisms of HIV.

2: How many of the people signing this list are scientists currently doing AIDS research, and doing new research that is currently being published.

Please… take your time.

308

sealamp,
How about the Durban Declaration? If you want to go petition-to-petition, I’m afraid we have you beat, old boy. It’s newer, larger by an order of magnitude, and signed by many more prominent scientists. The scientists who have signed the Durban Declaration have more often (by far) held their work up in front of their peers, and their peers have reviewed and accepted their work. The same cannot be said of the Perth declaration or the 1991 list.

I really admire your interpretation of our debate a few pages ago. It really takes some squinting to come to that view.

Here’s my recall of it. Perhaps a neutral third party can tell us which one is more accurate. Someone (I think Roger_Mexico) asked specifically for a cohort study which correlated AIDS symptoms to HIV positivity in a patient population that had never been treated by anti-retrovirals and exposed to risk factors. I think this was something Duesberg wants, so I searched and found something similar. The scope of the paper had nothing to do with actually showing an HIV>AIDS link; it was concerned with defining the sensitivity and specificities of clinical AIDS definitions in impoverished countries that did not have access to HIV tests. It took all of 30 seconds of searching, I posted it before I read it in very great detail, but on its own, taken for what it was written for, it is not a bad paper.

The researchers who wrote the paper were a little unclear in their defintions:

We have a debate on their definitions – specifically if someone can by PCR negative and still be classified as HIV+, or PCR positive and classified as HIV-. They don’t clearly say; I interpreted the definitions in one way, sealamp in another. They are both assumptions, and therefore both not worth debating scientifically.

I conceded that the researchers were unclear and I moved on. I understand their definitions, I understand your beef with their definitions. But in no way does this somehow diminish the fact that HIV infection leads to AIDS.

What you have done is pointed out some ambiguity in one paragraph out of hundreds of thousands of papers. You have not shown that the paper was fatally flawed, just pointed out ambiguity.

Here’s how it works. You have a contrarian idea. The onus is on you to provide data to support the contrarian idea first. I am not responsible for defending every ambiguity and research mistake in the 100,000 papers published correlating HIV to AIDS. These do not do anything to support your hypothesis, and actually does nothing to diminish the HIV>AIDS link (as you are not somehow by default supporting your contrarian hypothesis just by discrediting the first one). It is like the creationists – discrediting evolution science does nothing to lend automatic support for creationism.

Provide some data to support your hypothesis. Show a causative link between drug abuse, anal sex, and anti-retrovirals, and the acquired CD4+ T-lymphocytopenia of AIDS. Answer some of my questions.

Then, we can start to see if your hypothesis explains AIDS better than HIV. Follow Marshall’s and Prusiner’s path. That’s how science generally works.

309

Edwino writes:
“What you have done is pointed out some ambiguity in one paragraph out of hundreds of thousands of papers. You have not shown that the paper was fatally flawed, just pointed out ambiguity.”

I was attacking your scientific credibility in response to your attacking the dissidents’ scientific credibility. If you were truly credible as a scientist, you would have carefully reviewed some of those hundreds of thousands of papers and found at least one that clearly shows what you were trying to argue. And preferably BEFORE you formed your view which you were trying to argue. But instead, as you admit:
“I posted it before I read it in very great detail, but on its own, taken for what it was written for, it is not a bad paper.”

Perhaps you don’t understand that a paper can be written on HIV or AIDS (or both) and not establish that HIV is the probable cause of AIDS. Simply saying that there are hundreds of thousands of papers on HIV or AIDS doesn’t prove anything. You need to give a specific paper, or combination of papers, that establishes that HIV is the probable cause of AIDS. And when you do, please have ACTUALLY READ those papers. (I’d have hoped you would have read the papers BEFORE forming your conclusion that HIV is the probable cause of AIDS, but I guess it is too late for that.) You seem to have formed your opinion based on the sheer quantity of papers (“hundreds of thousands”) that have the words HIV or AIDS in them.

Astro writes:
“Hmmm… a ten to twelve year old list. Fascinating! Out of purest curiosity I wonder two things about this decade old list you have linked to-”

So how often do you want them to renew their petition?

Here is a link to a June 2003 - is that recent enough? - journal article which argues the dissident views, and answers many of the questions you have asked. Please ACTUALLY READ it:
http://www.virusmyth.net/aids/data/pddrchemical.pdf

310

Edwina,

 You are way off-base in your understanding of the actual events in Japan surrounding the SMON incident...here's the real story ;

http://www.virusmyth.net/aids/data/besmon.htm

 I agree with 'sealamp'... please actually READ it...perhaps you'll gain some insight into the "HIV" fiction.
311

I did read it. For a purportedly scientific paper about science in a supposedly scientific journal, it was a remarkable compendium of political jousting, old research, rhetorical games and anecdote. Not much (if any) relevant data mentioned regarding any current bio-medical HIV studies these titans of science were doing, but plenty of assertions that everyone else was on the wrong path. Quite a plum that they were able to get a paper pub’d in the Indian Academy of Sciences journal.

Interestingly the Deccan Herald had this to say

[sub]

[/sub]

Scientific peer review replaced by a jury system. This just gets better and better! I’m sorry. I can’t type anymore right now as I’m laughing so hard my fingers won’t stay on the keys.

312

Yaaaargh.

As I have stated, asking for one paper linked HIV to AIDS is just not going to happen. A multi-pronged, multi-field approach is taken in modern science in order to establish causation. I could show you papers showing a purification of the virus or an electron micrograph or anecdotal cases of AIDS where the only risk factor is HIV positivity or epidemiologic studies correlating HIV with AIDS, or molecular genetic papers unfolding how HIV causes T-cell cytotoxicity. None of these papers will please you, because none of them alone show absolute causation by itself. We are talking about a body of work, not just one paper.

The paper I produced is one tiny piece of the puzzle. It showed a very sick, septic populations of infants, and showed that a strictly clinical definition of AIDS was nearly 100% specific in picking out the ones that were HIV+. It is was a quick way to respond to Duesberg’s call for a cohort study of outcomes between populations with no risk factors and the only difference being HIV status. This is what the paper showed, to some degree.

Of course, you attempt to nitpick their definition to pieces. The kids were given different workups when they arrived at the ER. Most, it appears were tested by PCR twice. Some were tested only once and had clinical symptoms of AIDS. These were classified as HIV+. The ones who were negative were PCR- (regardless of ELISA). I have asked you multiple times how one could be PCR+ without having HIV infection, and you have said that I have misinterpreted the definitions. I disagree completely – their definitions only dealt with clinical symptoms if the child was PCR+.

This is really an “angels on the head of a pin” thing. This is one paper, which deals rather nicely with one small aspect of the problem. What you are putting at issue is beyond this one paper, which I admittedly took out of its scope.

Say what you will about me as a scientist, I have thicker skin that to get irked about comments on a message board. I know my research has gone through peer review and has been approved by my fellow scientists. Impressing you is not really an issue.

What you are putting at issue is the entire field, the tens of thousands of papers that have been peer reviewed. Again, it is not my responsibility to defend every single one of them. I am not an AIDS biologist, and I have never published on the HIV/AIDS causation. From the primary papers I have read, from the data out there, the link has been established, and I believe it for three reasons:
a) The link stands up to scientific scrutiny (apart from the dissent crowd) by researchers who have more background than I.
b) One can use the link to make very good predictions about the clinical course and the progression of the disease, treatment of the disease, and steps to prevent the disease. These predictions have held up, and now AIDS is an avoidable and treatable disease.
c) There is just no better theory out there that explains the data.

So, I have repeatedly asked for you to produce some data to answer c), such that we can move towards a) and b). And now you produce the Duesberg J Biosci paper, which is mostly a review article published in a decidedly fifth-rate journal. I have read the paper in some detail, and admittedly he tries to address some of the questions I have presented. I don’t think he does it very well, though.
1,2) (risk factors->CD4 decline, dose response->CD4 decline) He states that drug use rates mirror AIDS rates; he states that AIDS defining diseases are caused by illicit drugs by “summarizing the evidence from 60 publications since 1909 which prove that illicit recreational drugs cause all AIDS defining … diseases at time and dose-dependent rates.” He cites two of his papers, I will track these down. His entire argument rests of synchronicity of drug use rates and AIDS cases in the early 1980s. Not a word on CD4+ T-cell specificity.
3) (ICTL) Nothing.
4) (no risk factor AIDS) Well, everything is a risk factor. Everybody has risk factors! Haemophiliacs – they had antiretrovirals. Lab workers – they didn’t accurately ask each one of them how much homosexual sex they were having. They could have all been popper addicts. And they got AZT! How can we link to AZT? Again, by synchronicity of deaths 10 years after dosage rates.
5) (HAART) Mainly focuses on AZT, which hasn’t been used in HAART monotherapy for 7 years (I am talking about HAART, not AZT prophylaxis). AZT monotherapy was never a good therapy. Surprisingly, he doesn’t talk about protease inhibitors at all. Hmmm…
6) (risk factors and clinical course) He depends almost entirely on synchronicity.
7) (risk factors and lab findings) Never mentions CD4 T-lymphocytopenia at all.
8) (treatment by risk factor abatement) No mentions. He does cite a study that one of the authors has conducted, which is incredibly tricky and misleading:

Issues with this – they were only classified by HIV antibody status, which all clinicians should know is an incredibly poor method of defining HIV status. So we don’t actually know how many are actually HIV+. Seond, all 3 of the deaths occurred in 18 patients who have seroconverted before 1993. 4 of these actually have AIDS, as defined by CD4+ counts below 200. 3 more have counts below 500. Normal is above 500. The other 8 patients have no CD4 count listed. So what can we say about the patients who have had latency greater than 10 years and have CD4 counts listed. 3 of 10 are dead, 4 have AIDS, 3 are on their way to AIDS. None can be classified as normal.

How about the patients with latency under 10 years? There are 18 of these as well. None have died, but 5 of the 12 with listed CD4 counts actually have AIDS as defined by CD4<200. Only 2 have counts above 500, with 2 more between 400-500 (borderline normal). So 4 of 12 are still OK, and the rest have AIDS or are close to it. Again, let me reemphasize that his standard of establishing HIV positivity, HIV antibody status by itself, is not a good way of actually telling if these people have HIV infections. So the normal people may not actually even have an HIV infection.

Getting off of the drugs and away from the risk factors doesn’t do all that much, it seems.

So, in conclusion, what are we left with? If we are going to accept all of this paper as fact, Duesberg adequately shows that drug use has been somewhat synchronous with AIDS rates, if you shift the peaks by a few years. He hasn’t provided a mechanism, he hasn’t specifically defined risk factors or what they may have in common (how do AZT, amyl nitrite, heroin, cocaine, malnutrition, malaria, poor drinking water, vaccines, and anal sex all cause a common pathology?), and he hasn’t demonstrated that the HIV/AIDS link is even that tenuous. He has made some predictions, but has done no science to show that they are correct.

Not so good, eh?

313

Duesberg is full of shit if he thinks that he is being discriminated upon based on his HIV/AIDS stuff. His aneuploidy stuff is still published regularly: he has 10 papers since 2000. That’s pretty good – I know a lot of professors who could only hope to match that.

314

Edwino writes:
“5) (HAART) Mainly focuses on AZT, which hasn’t been used in HAART monotherapy for 7 years (I am talking about HAART, not AZT prophylaxis). AZT monotherapy was never a good therapy. Surprisingly, he doesn’t talk about protease inhibitors at all. Hmmm…”

Yes he does talk about Protease inhibitors, for instance see the section marked (ii) in the second column of page 396. I again ask you to ACTUALLY READ the article.

Edwino writes of Table 8 in the article:
“4 of these actually have AIDS, as defined by CD4+ counts below 200…”

The table is not clear on the issue, but I think those CD4 counts were from time of diagnosis of HIV (or AIDS). In that case your analysis is based on a misinterpretation.
Look, in discussing the table Duesberg et. al. write:
“In an effort to obtain independent proof that abstaining from anti-HIV drugs and recreational drugs is sufficient to survive HIV-infection or even to recover from AIDS, one of us, CK, in 1985 initiated a study of AIDS
patients from Kiel, Germany, who have volunteered to abstain from anti-HIV treatments. Remarkably, only 8%
(3 of 36) of the patients not treated with anti-HIV drugs have died since their HIV antibodies were first detected, two of them 16 years and one 10 years after their first diagnosis of antibodies against HIV (table 8). Most have recovered from their initial AIDS-indicator symptoms. By contrast, 63% of all German AIDS patients (11,700 out of 18,700) of which most were treated since 1987 with anti-HIV drugs have died (Robert Koch Institut
2000). Thus our relatively small sample supports the hypothesis that without anti-HIV drugs and/or recreational
drugs HIV fails to cause AIDS. Indeed without drugs AIDS patients recover, despite the presence of HIV.”

That last sentence is: “Indeed without drugs AIDS patients recover, despite the presence of HIV.” I think we should interpret that to mean that patients like the “4 of these [that] actually have AIDS, as defined by CD4+ counts below 200…” you point out HAD AIDS in 1985 (the start of the study) but then recovered during the followup period (without medication). Or something like that. Why would he say AIDS patients recover if during the followup they still had (or got low enough CD4 to have) AIDS? Clearly these must be the CD4 counts at the start of the study. Duh.

I don’t know what you are trying to argue elsewhere - it doesn’t look like you spent much time writing your arguments. They look like a stream of conscious outline one might write before posting a coherent argument.

Edwino writes:
“Duesberg is full of shit if he thinks that he is being discriminated upon based on his HIV/AIDS stuff. His aneuploidy stuff is still published regularly: he has 10 papers since 2000. That’s pretty good – I know a lot of professors who could only hope to match that.”

I think he says his HIV/AIDS stuff is being supressed, not all of his work. If he is so good at getting papers published as you admit, Edwino, why wouldn’t his papers on HIV/AIDS also be of publishable quality?
I quote from the article:
“For example, an early precursor of this article was written in response to an open invitation from a pharmacology journal over 3 years ago. But, after considerable pressure on the journal from anonymous AIDS
experts, the editor requested a reduced article, which was neither accepted nor rejected. Instead, the editor simply dropped all further correspondence. Subsequently, the editor of a prestigious German-based science journal invited another precursor of this article 2 years ago, which received two favourable reviews in short order. But before the manuscript could be revised, the editor informed us that the publisher was concerned about losing subscribers if our paper were published and ceased all further correspondence. It is this passive resistance that can grind down even the most determined truth seeker.”
Two favorable reviews but dropped for fear of losing subscribers? Is this the way a prestigious science journal should work?

315

Edwino writes:
“5) (HAART) Mainly focuses on AZT, which hasn’t been used in HAART monotherapy for 7 years (I am talking about HAART, not AZT prophylaxis). AZT monotherapy was never a good therapy. Surprisingly, he doesn’t talk about protease inhibitors at all. Hmmm…”

Yes he does talk about Protease inhibitors, for instance see the section marked (ii) in the second column of page 396. I again ask you to ACTUALLY READ the article.

Edwino writes of Table 8 in the article:
“4 of these actually have AIDS, as defined by CD4+ counts below 200…”

The table is not clear on the issue, but I think those CD4 counts were from time of diagnosis of HIV (or AIDS). In that case your analysis is based on a misinterpretation.
Look, in discussing the table Duesberg et. al. write:
“In an effort to obtain independent proof that abstaining from anti-HIV drugs and recreational drugs is sufficient to survive HIV-infection or even to recover from AIDS, one of us, CK, in 1985 initiated a study of AIDS
patients from Kiel, Germany, who have volunteered to abstain from anti-HIV treatments. Remarkably, only 8%
(3 of 36) of the patients not treated with anti-HIV drugs have died since their HIV antibodies were first detected, two of them 16 years and one 10 years after their first diagnosis of antibodies against HIV (table 8). Most have recovered from their initial AIDS-indicator symptoms. By contrast, 63% of all German AIDS patients (11,700 out of 18,700) of which most were treated since 1987 with anti-HIV drugs have died (Robert Koch Institut
2000). Thus our relatively small sample supports the hypothesis that without anti-HIV drugs and/or recreational
drugs HIV fails to cause AIDS. Indeed without drugs AIDS patients recover, despite the presence of HIV.”

That last sentence is: “Indeed without drugs AIDS patients recover, despite the presence of HIV.” I think we should interpret that to mean that patients like the “4 of these [that] actually have AIDS, as defined by CD4+ counts below 200…” you point out HAD AIDS in 1985 (the start of the study) but then recovered during the followup period (without medication). Or something like that. Why would he say AIDS patients recover if during the followup they still had (or got low enough CD4 to have) AIDS? Clearly these must be the CD4 counts at the start of the study. Duh.

I don’t know what you are trying to argue elsewhere - it doesn’t look like you spent much time writing your arguments. They look like a stream of conscious outline one might write before posting a coherent argument.

Edwino writes:
“Duesberg is full of shit if he thinks that he is being discriminated upon based on his HIV/AIDS stuff. His aneuploidy stuff is still published regularly: he has 10 papers since 2000. That’s pretty good – I know a lot of professors who could only hope to match that.”

I think he says his HIV/AIDS stuff is being supressed, not all of his work. If he is so good at getting papers published as you admit, Edwino, why wouldn’t his papers on HIV/AIDS also be of publishable quality?
I quote from the article:
“For example, an early precursor of this article was written in response to an open invitation from a pharmacology journal over 3 years ago. But, after considerable pressure on the journal from anonymous AIDS
experts, the editor requested a reduced article, which was neither accepted nor rejected. Instead, the editor simply dropped all further correspondence. Subsequently, the editor of a prestigious German-based science journal invited another precursor of this article 2 years ago, which received two favourable reviews in short order. But before the manuscript could be revised, the editor informed us that the publisher was concerned about losing subscribers if our paper were published and ceased all further correspondence. It is this passive resistance that can grind down even the most determined truth seeker.”
Two favorable reviews but dropped for fear of losing subscribers? Is this the way a prestigious science journal should work?

316

Sorry, sealamp, but you lose. You can even have my pity if you want it.

Esprix

317

sealamp

A few things. First, I read the paragraph about protease inhibitors but it makes no sense. He claims HIV protease inhibitors inhibit cathepsin D, an aspartic protease in the same family as the HIV protease. He cites a Deeks JAMA review and some calculations he has made. First, the Deeks paper says no such thing. Second, there is no literature out there showing that HIV protease inhibitors inhibit cathepsin D. Third, the transgenic knockout mouse for cathepsin D shows anorexia and immune deficiency (albeit not specific CD4 cell decline), which he states are AIDS defining symptoms. The transgenic mouse is not a human.
a) The HIV PIs were FDA approved, which includes testing in normal subjects. No anorexia and immune deficiency was reported at antiviral doses.
b) The HIV PIs along with nucleoside analogs are given to untreated AIDS patients who are exhibiting those symptoms and the symptoms go away. It makes no sense to claim that the PIs are causing them. Duesberg’s argument makes no sense whatsoever.

Next, the CD4 business. CD4 declines were first described in 1988, and CD4 counts only became routine well after that. So the CD4 counts on the patients from 1985 certainly were not done at presentation. As for the rest, that’s anybody’s guess. I don’t think it is likely, but the description is ambiguous more than anything. Given the amount that you have (wrongly) jumped on me about definitions in the J AIDS paper, at least pretend to be fair. At least give a face on using the same scientific standards you are using the piece the HIV/AIDS literature apart on the Duesberg paper. You will find that it crumbles entirely.

You haven’t addressed the major concern of the paper. Everything comes down to his argument for synchronicity. Drug use and AIDS are synchronous (shifted by some years). AZT use and AIDS are synchronous (shifted by some years). “Gay liberation” and AIDS are synchronous (shifted by some years). It is perhaps the weakest epidemiologic argument. I can show all kinds of things are synchronous with AIDS – global warming, viewership of Friends, personal computer usage, investment in the stock market. Care to address that, the major issue raised in the paper, rather than my critical thinking ability?

318

allengraves2003,

As I have stated elsewhere in this thread, I will not address virusmyth pages. We have a perfectly good liturgy of medical documentation, find me real cites if you want to argue.

I did look at the virusmyth page on SMON though, because of the dearth of availible stuff on it. There are 74 PubMed listings on it in English (with another 130 in Japanese, which I don’t read), with only 8 mechanism papers in the last 10 years. So I broke down and looked at virusmyth. It states exactly what I said – it was a small epidemic, published in a relatively closed medical community, not seen outside of Japan. It was first described in the late 1950s, and it took them a little over 10 years to trace down the aetiology, by 1970. It eventually was traced to drug toxicity, namely clioquinol, an oral antibiotic given mostly for amebiasis.

This is the reason we have agencies like the FDA. The FDA has prevented tragedies like this and thalidomide in the USA, and has become a model of drug approval agencies worldwide.

There is no similarity to HIV/AIDS here. A small outbreak in the 1960s in Japan, followed by a controversy discussed only in Japanese language neurology journals, is not the same thing as a global pandemic with research on a global scale. 1960s medicine is not the same as 21st century molecular diagnostics.

What’s more is that the Japanese scientists were always willing to admit that their virus of the month was not a good disease candidate. First, it was an echovirus which could not be isolated from all patients and caused no disturbance in animal or cell culture models. Then, a Coxsackie virus that proved to be a lab contaminant. Then, post-hoc, after the aetiology was pinned down, a lone scientist pushed a herpes virus, which again did not replicate disease in animals. According to virusmyth, they became fixated with the virus idea. But they could never explain the disease with a single virus, and always had to go looking for another one until they found clioquinol. This doesn’t apply to HIV/AIDS: HIV causes the disease in model systems, 100% of AIDS patients have AIDS, all reports show that HIV+ individuals left untreated develop AIDS, treating HIV treats the disease, and the HIV lifecycle has been linked molecularly and genetically to the specific CD4+ T-cell die off that characterizes AIDS.

Again, IMHO this has no bearing. Please explain to me how you think it does.

Sorry about butchering your userid. It was unintentional.