A Scientist debates an AIDS patient

Gos,
I have no problem exchanging points of view and the supporting material with you over e-mail. If you wish to post it up later on the board I am ok with that as well. The problems I have, however, are the failing to post (for whatever reason) replies.
I agree to your terms and find them fair:

You get to do the same however, and prove using scientifically correct sources that such viral genomes are in fact normal and harmless parts of the human genetic material.
I should however like to make two points clear.

1) I did not state that anyone "without my level of knowledge is incompetent".
What was meant was that in order to understand the data presented in scientific papers one must have at least a general understanding of the subject. I could not argue the validity of a paper on String Theory with a physicist since I do not have the background in said subject and any assumptions I make would be likely due to my error in understanding. This is akin to the people who use the "melting point of steel" argument to support their claim that the fires in the WTC could not have caused the collapse. They may hear what seems like convincing arguments from one side that sound good but are completely incorrect. This is something I would like to avoid.

2) The reference to the Dunning-Kruger effect is not at all meant as an insult.
It is however my observation that many of the comments made on that site demonstrate a lack of basic understanding in genetics and biology. As I stated, I admit I do not know everything. I would be a fool to claim I do. I have an open mind in science as it is evidence and fact which must dictate reality, not our preset beliefs, regardless of their origins.

Lastly, I would like to clarify one thing that you had posted in your last, lengthy post. I did not claim that HCV caused cervical cancer. That was a reference to HPV. That said, if we both agree on the rules set forth then lets begin. Please bear in mind that I do have a full time job so responses may take a little bit to come.

Cheers
-BioLab

Jean-Marc wrote: "The problems I have, however, are the failing to post (for whatever reason) replies"

Yeah, I agree. This is something I've criticized the AME moderators for to no end. Personally, if I had my way, they'd only censor ad hominem attacks. It doesn't do anyone any good to limit the debate, and if the AIDS orthodoxy hadn't been censoring dissent for 20 years now, we'd probably have a lot better idea of the nature of AIDS, even if we dissidents are wrong. Science is never ill-served by free debate, but it is often stymied by censorship.

Jean-Marc wrote: "You get to do the same however, and prove using scientifically correct sources that such viral genomes are in fact normal and harmless parts of the human genetic material."

I have never made any such claim.

On the larger issue of viruses, I used to believe in them, and now I am agnostic. I literally don't know what to think. However, if you'd like to have such a discussion with someone who has made quite a study of the subject, "Softrat" in the AME forum makes a rather interesting case, using the conventional published literature. Perhaps you should pose the same question to him.

On the issue of HIV, I make no claim to knowledge of what HIV is. For all I know, it might well be a retrovirus, or it might be harmless bits of normal human genetic material, or it might be nothing more than a lab artefact -- non-infectious particles that are mass-produced by Gallo's co-culture techique, and which don't exist in the subject's blood or tissues at all. (Personally, I strongly suspect that the last option is the correct one, but if I saw convincing proof otherwise tomorrow, I would reconsider my opinion on the matter.)

If HIV is actually a retrovirus, that still doesn't address the issue of whether it causes AIDS. Most if not all retroviruses are harmless, and for that matter, how do we know that HIV is not merely an opportunistic infection? When a patient is riddled with various OIs, how do you determine which are the symptoms of AIDS and which is the cause? I have done quite a bit of research, and I have yet to have seen the paper that convincingly answered that question in the case of HIV. On the contrary, we're still being told that three lab workers who stuck themselves with contaminated needles 20 years ago are the evidence that HIV fulfills Koch's Postulates. (See the NIH/NIAID publication, The Evidence that HIV Causes AIDS) Where I come from, that's anecdotal evidence, yet NIAID director Dr. Anthony Fauci says that this anecdotal evidence is enough for him, and no further scientific study is needed. (See The Duesberg Phenomenon, Jon Cohen, Science 1994 -- if you want a link to the entire article, I can provide it.)

Jean-Marc wrote: "What was meant was that in order to understand the data presented in scientific papers one must have at least a general understanding of the subject."

I'm not a biologist, however, I do at least have a general understanding of the concepts involved, and have read quite a number of scientific articles on the subject of HIV. At first, I used to get bogged down in terminology and concepts that I didn't understand, but that rarely happens anymore.

However, you must understand that when you cite the Dunning-Kruger effect, and when you enter a discussion by demanding whether any of the participants are degreed professionals, it's kind of hard not to get the impression that you're questioning the competence of others. If that is not what you intended to imply, then I am at a loss for what to infer.

Jean-Marc wrote: "I did not claim that HCV caused cervical cancer."

That would be my bad. I have a tendency to spit out the wrong words sometimes. I'll say "east" when I mean "west", I'll say "HCV" when I mean "HPV"; it happens all the time. In my own mind, I know what I mean, but for some reason I'll open my mouth and the wrong term comes out. (Interestingly, I never say "north" when I mean "south", but I almost invariably say "east" when I mean "west", and vice versa.) Feel free to correct me, or to ask for clarification, should I say something that doesn't seem to make sense.

Jean-Marc wrote: "That said, if we both agree on the rules set forth then lets begin."

Okay.

For starters, (if you don't mind me dictating the starting point of the discussion), I'd like to ask what facts convince you 1) that HIV exists as a single, unique, exogenous retrovirus, which is present in the blood of all AIDS patients, and 2) that HIV plays a causal role in AIDS (as opposed to being merely an opportunist or harmless passenger virus.)

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

Gos,

Glad to be having a civil conversation with someone. You are correct that it was SoftRat that claimed HIV was a normal part of the human genome. This is my mistake. Also, if anyone including you took offense to the education comment then I apologize. It was not my intention. I will also offer this to you; if at any time there is something you do not understand or feel you misunderstand please ask. I have taught biology at the University when I was doing my masters and have no problems explaining areas of confusion. Also, spelling errors (especially on my part) are a pet peeve of mine. If you notice any in my writing please point it out so I can be more careful. Now let me get to your questions.

1) For starters, (if you don't mind me dictating the starting point of the discussion), I'd like to ask what facts convince you 1) that HIV exists as a single, unique, exogenous retrovirus, which is present in the blood of all AIDS patients

I will repeat here a part of the post that was moderated out as I feel it is relevant to this issue.
Certain pathogens can produce strikingly similar symptoms to others. It is a logical fallacy to say "Since AIDS is a depression of the immune system, and HIV is believed to cause AIDS, thus HIV must cause ALL depressions of the immune system." This would be as much an error as stating “since Robber-X binds and gags all his victims, if a victim is found bound and gagged, it must be Robber-X that did it”. The obvious problem here is that someone could have copied his MO. Pathogens (and yes toxins, too) can mimic the symptoms of diseases. An example would be diarrhea. To say that amoebic dysentery causes diarrhea is absolutely correct. However, if someone then challenges that belief by stating you must produce amoeba in every case of diarrhea to prove you are correct, there will be some obvious problems.

Thus the term AIDS is generally accepted to refer to immune suppression caused by the actions of the HIV virus not by other causes. Question 1 pretty much feeds directly to question 2.

2) “…that HIV plays a causal role in AIDS (as opposed to being merely an opportunist or harmless passenger virus.) “

I will start with “HIV fulfills Koch’s Postulate” .

(This first part references “Koch.PDF”)

While Peter Duesberg has argued against this (and it appears that much of the “dissident” movement in based on his arguments), they have been shown to be either inadequate or flat out incorrect in many cases. Some of his arguments were based on old or outdated data. As an example, look to page 17 (although I suggest reading the whole article, it is easy to read and has much good information). Duesberg argued that HIV cannot be isolated in 20%-50% of AIDS patients. This was claimed on what was, even at that time, outdated data. I saw this claim still being posted on AIDS-Myth boards recently (although I honestly don’t know if it was the one you were on or a different one).

There are many examples of studies supporting the fulfillment of Koch’s Postulate but I will list only a few:

Case 1) The 3 lab workers most cited are not the only examples of occupational transmission. CDC reports in 1999 56 health care workers with no other risk factors who contracted HIV occupationally. At the time of publishing, 25 of them had already progressed to AIDS (I’m still trying to track down the complete reference for this, sorry)

Case 2) Eleven infants with no other risk factors developed AIDS after a one time exposure to serum donated by a single HIV+ individual. (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=8193497&dopt=AbstractPlus)

3) Perhaps one of the most damning is a study of 715 homosexual men with similar lifestyles and habits. AIDS ONLY developed in those who were positive for the HIV virus and NEVER in those who were HIV-. To rephrase, HIV was the ONLY predictive factor in the development of AIDS in these subjects. Lifestyle and drug use were similar in both HIV+ and HIV- groups. Duesberg claims that AIDS is likely caused by recreational drug use. (See http://www.duesberg.com/) This is outright refuted by the data in this paper. At the time this paper was published, not all of the HIV+ men had yet developed AIDS and if you find a follow up article mentioning the remainder please let me know as it would be interesting. Please note that a 715 people study is not considered anecdotal evidence :-P

(http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=8095571&dopt=AbstractPlus)

4) Animal models (Chimps) infected with HIV developed immune suppression and AIDS and cell-killing is likewise observed in mice models with SCID and a human immune system. (also trying to track down the links for these two).

5) In models using the closely related virus SIV, injection of naked plasmid DNA containing the SIV genome lead to AIDS.

(http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10195754&dopt=AbstractPlus)

6) A Florida dentist who transmitted the HIV virus to six of his patients (genetic analysis indicated the very strong likelihood that he was the source). The dentist and three of the patients developed AIDS and died. A fourth developed AIDS but had not died yet as of the publishing of this paper and the last had not yet developed AIDS. The papers state that 5 of the 6 patients had no other risk factors for HIV (my guess would be that this included recreational drug use).

(http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=7978703&dopt=AbstractPlus)

Please note that I have seen the arguments before that HIV does not infect enough T-cells to cause suppression of the immune system. Not only is this refuted by many studies (including those in #3 and 4) but it has been long ago determined that a simple lyse-to-kill strategy is not the only method of T-cell killing. If you have time, read up on HIV mediated formation of syncytia. Other than making for an interesting read, it also provides insight on T-cell depletion mechanisms.

-Cheers,

BioLad

OK I told you I was still looking for some of the reference papers. Here are a few links

Here is a link to at lest one paper showing that "lyse-to-kill" is not the only mechanism for T-cell death" This is a full access article
(http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=446229&blobtype=pdf)

Here is one article using SCID mice with human immune systems with HIV. Also full acces:
(http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=166415)

A second one on SCID mice, full access:
(http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=1865151&blobtype=pdf)


A SCID mouse experiment where they used mutated HIV to test the effects of the mutations on T-cell depletion (click PDF in upper left side for full):
(http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=110051)

I'm still trying to find time to get the references to the health care workers. In the mean time the above papers should demonstrate conclusively that HIV does in fact cause T-cell depletion.


-Cheers,
BioLad

Jean-Marc wrote: "I would however recommend reading the Koch’s Postulate paper because it provides a very fair analysis of the claims made by Duesberg. Reading it taught me a few things I did not know as well."

I will read it, then. If for no other reason, then that I would be quite interested to read anything that provides a fair analysis of Duesberg, since I have yet to read any article, dissident or orthodox, that does so. Typically, his detractors tend to be unfair in the extreme, and his supporters are just as bad if not worse. (I myself am only partially a supporter, since I do not consider all of his conclusions to be necessarily valid, but I do note that his documentation tends to be exceptionally superb.)

Jean-Marc wrote: "One thing to realize about science is that rarely if ever will a person make a claim to 100% accuracy on any test. This is not only bad science but, in cases of tests that can impact a person’s life as much as an HIV test can, a matter of legal liability."

This is quite an important point, even if it is not directly relevant to our debate, given the current political climate in which being HIV-positive can be a legal liability in and of itself (not to mention the associated social stigma, etc.), due to the criminalization of certain acts, including consentual sex, for HIV-positives, which are not criminalized for HIV-negatives.

Jean-Marc wrote: "So, can I supply literature or a test pamphlet showing no errors in ELISAs? No, of course not. I would be a fool and a liar to claim this as would anyone else."

Interestingly enough, I can supply such literature, (apparently published by fools and liars, by your account, and I thank you for pointing this out) though I must qualify this statement by pointing out that this is based not on the demonstrated correlation between the test and actual HIV, but on the demonstrated correlation between one test and another test (which itself was never demonstrated to correlate to actual HIV infection.) Thus, in the literature I could supply, Heckle and Jeckle are shown to be 100% in agreement, but there's nothing to suggest that they're both telling the truth.

Jean-Marc wrote: "Current HIV ELISAs are however measured at between 99.5% and 99.9% accurate. Meaning that even at only 99.5% accuracy, statistically, of the 365 HIV+ men in that study, 363.175 would have the HIV virus. I’m sure you would agree that this would not have an effect on the validity of the conclusions of the report."

If there were any validity to your math, I would certainly agree. However...

I hate to make an accusation such as the one I am about to make, of someone with a masters in biology, as it seems somehow disrespectful and condescending. Nonetheless, I must point out that here you are demonstrating at best, a layman's grasp of how "accuracy" is measured for a test.

Indeed, the term "accuracy" is never used; instead, the terms "sensitivity" and "specificity" are the accepted terms for any discussion of a test's "accuracy", and this applies not only in science, but in mathematics as well.

And, as I am about to demonstrate mathematically, your math, being based on a poor understanding of the concepts involved, is inherently flawed and therefore specious.

Definition of terms:

Sensitivity: The ability of the test to correctly detect when a condition is true, vs a false negative. Example: If 1,000 HIV-positives were tested using a test with 99.5% sensitivity, 995 of them would test true-positive, and the other 5 would test false-negative.

Specificity: The ability of the test to correctly detect when a condition is false, vs a false positive. Example: If 1,000 HIV-negatives were tested using a test with 99.5% specificity, 995 would test true-negative, and 5 would test false-positive.

Specificity/sensitivity gap: To my knowledge, I am merely making this term up for the sake of shorthand, but in this discussion, I am using it to refer to the difference between 100% and the sensitivity or specificity of a given test. Thus, a test with a specificity of 99.5% would have a specificity gap of 0.5%

Baye's Theorem dictates that when mass testing is done in a population in which the incidence of a condition is low, a significant number of positives will be false positives. Furthermore, where the actual incidence is lower than the specificity gap (as defined above) of the test in question, more than half of all positive results will be false positives, and where the actual incidence is nil, 100% of all positives will be false positives.

Now, taking these concepts as defined above (feel free to check the definitions of all but the specificity gap, which, as I said, I'm using here merely to save keystrokes,) let's do a hypothetical test of a randomly-selected group of 100,000 average Americans:

According to the CDC, there are 1.2 million HIV-infected Americans. According to the US Census, there are 300 million Americans. 1,200,000 / 300,000,000 * 100 = 0.4% seroprevalence. Therefore, in a group of 100,000 randomly-selected Americans, we would expect about 400 of them to be HIV-positive (assuming the validity of the CDC estimates, which I don't, but I digress.)

Now, let's do our hypothetical test, using a test with 99.5% sensitivity and specificity (since 99.5% is the "accuracy" you cited in your example where you said there would only be 1.825 false positives.)

400 HIV-positives * 0.5% sensitivity gap = 2 false negatives, 398 true positives

99,600 HIV-negatives * 0.5% specificity gap = 498 false positives, 99,102 true negatives

Thus, according to Baye's Law, in a population with a 0.4% seroprevalence, tested using a test with 99.5% sensitivity and specificity, we would expect false positives to outnumber true positives by a ratio of approximately 1.25:1.

This is, you will concede, an enormous difference from your example, where, using "lazy math", you would have estimated only 2 false-positives, out of 400.

Now, of course, I'm sure that at this point, you suspect that I am somehow cooking the figures. Look up the concepts involved, and do the math for yourself. I will concede that by using your lowest specificity estimate, I cheated in a small way, in that if I'd used the 99.9% estimate instead, the ratio would have been closer to 100 false positives for every 400 true positives. Even so, as you can see, this still would mean that 20% of the total number of positives would be false positives, not 0.1% as your logic would suggest. Thus, my point still remains valid, in that this still is a significant number of false positives, and no less than 200 times as many as you would estimate for a test with 99.9% "accuracy", using what appears to be a layman's grasp of the concepts involved.

Now, the devil is in the details, and there is no exception in the case of Baye's Law. For example, if the actual incidence were much higher, the number of false positives would fade significantly, to the point of statistical insignificance, assuming a high enough incidence. It is for this reason that doctors are typically reluctant to test anyone not in a "risk group", while those perceived to be "at risk" are tested frequently, since the test would theoretically tend to be more accurate in a population with (what is presumed to be) a high incidence.

However, this is specious reasoning, since it is based on the assumption that false positives will not occur as frequently among those "at risk" as among those in "low risk" groups. In reality, if we would expect to see a certain percentage of false positives in a group with no risk, then we should expect to see a comparable percentage of false positives among HIV-negatives in the very "highest risk" groups. This concept is never addressed within the mainstream medical community, and as a result, virtually all positives in "high risk" groups are assumed (making an ass out of u and me) to be true positives, while virtually all positives in "low risk" groups are assumed to be false positives. This is pure prejudice, plain and simple, with no rational scientific or mathematical basis.

Now, having demonstrated that 20%-55% of positive HIV test results are actually false positives (based on a specificity range of 99.5%-99.9%), I do not concede that the remainder are true positives; I am merely indicating the minimum percentage of false positives that can be expected, according to established mathematical models. The burden of proof remains upon you to prove that the remainder are true positives.

This can only be done by establishing that HIV tests have been validated against the gold standard of actual viral isolation. I contend that this has never been done, but you are certainly free, as I said before, to attempt to prove me wrong, by supplying literature to the contrary.

Failing the use of such a gold standard, there is no basis for us to arrive at any figure concerning sensitivity and specificity, since these figures are based on assumptions, rather than on demonstrated facts. Therefore, for all we know, sensitivity and specificity might be any value, even zero.

As to the definition of viral isolation, I do not accept Gallo's "co-culture" technique as a surrogate for actual viral culturing, since it is entirely possible that Gallo's process (which he invented for the sole purpose of allowing him to "detect" a virus which cannot be detected in the lab by any other means,) may produce only reproducible lab artefacts, which do not correlate to any actual virus found in the subjects' tissues. However, for the sake of argument, I shall indulge (on a purely hypothetical basis,) Gallo's co-culture technique for the next few paragraphs.

Earlier this year, Gallo testified in a criminal appeals case in Adelaide, Australia, involving a man who had been convicted of spreading HIV. (COURT OF CRIMINAL APPEAL, Hon SULAN J, NO.65/2006, R V ANDRE CHAD PARENZEE, MONDAY, 12 FEBRUARY 2007, 10.04 A.M.)

In his testimony, Gallo said, "Let me tell you something that we didn’t publish... We received blinded, that is coded, samples to do the antibody testing on and we tested and those we got positive they sent out the blood cells along with controls from normal donors that were not infected. We isolated HIV from every case that was antibody positive." [This "isolation" could only have been done by co-culture, since Gallo was unable to isolate HIV by conventional culture in nearly 2/3rds of AIDS patients (see Gallo, Science, May 1984 -- I forget the title, but it's 1AM and I'm too lazy to look it up at the moment, but it was the very first paper Gallo ever published on HIV.)]

Now, I'd like to take a moment to address the issue of Gallo's "evidence" being unpublished. In science, unpublished evidence is considered a null, but as I will concede (and I'm sure you'll agree,) this does not necessarily indicate that it is not true, since 100% of all human knowledge was at one time unpublished, and 100% of the objective facts that we don't know remain unpublished to this day.

Nonetheless, the fact that Gallo never published this finding makes it untenable as scientific evidence, so if we are to find scientific evidence that HIV can indeed be isolated from everyone with HIV antibodies, we are forced to look elsewhere.

The fact, however, that Gallo was forced to cite unpublished evidence in court, indicates with almost 100% certainty that if any such experiments have ever been conducted and the results published, Gallo does not know it, or he would have cited those experiments instead.

Now, the fact that Gallo doesn't know of any such studies does not necessarily prove that such a study could not possibly exist, since it's virtually impossible for one man to know 100% of the literature on AIDS. However, we are talking about the co-discoverer of HIV, and as such, it would be an understatement to say that he would have more than a passing interest in the subject. Thus, the fact that Gallo knows of no such study strongly suggests that no such study exists (though, as I said before, you are eagerly invited to attempt to prove otherwise.)

Now, as to the question of whether Gallo ever performed such experiments, and whether the results were as he testified them to be, we can only consider the credibility of the source, since we have no other measure by which to judge his statements, those experiments (if conducted) having gone undocumented.

Gallo, unfortunately, is hardly unimpeachable. I will not claim that this is not the first time Gallo has been caught in a lie (since I know this to be untrue,) but only because it would be too long a tale to tell. Instead, I will conclusively prove that it's not the only time Gallo was caught in a lie that very day, in that very courtroom. (I actually can claim legitimate credit for having been the one to catch Gallo in this lie, having done so only two days ago, and having been since contacted by prominent dissidents, some with PhDs and far more extensive knowledge than my own, who marveled that no one had picked up on it before.)

In an article, (a rebuttal to Celia Farber's 2006 article in Harper's, entitled Out of Control), dated March 25, 2006, authored by Robert Gallo, et al, it is stated:

"Farber quotes Valendar Turner's letter which makes the same misrepresentation about nevirapine not being tested against placebo discussed above. As explained above nevirapine clearly performed better than placebo, despite Turner’s allegations. Of note is that Turner is a prominent AIDS denialist in his own right, so is scarcely an objective reviewer of the trial data." (P. 30, 46; 3)

The article goes on to say:

"Farber quotes Turner referring to a study of 561 people. We are not sure what the 561 person study is that Turner refers to." (P. 30, 47; 1)

However, less than a year later, when Gallo testified in the Parenzee appeal case, he pretended not to know who Valendar Turner was, and denied having ever even heard of him:

"By the way, can I ask you who is Dr Turner? I didn’t have a chance to really study who he is. I have never heard of him before." (P. 1272)

Now, I will concede that this does not conclusively prove that Gallo lied about his unpublished experiments. However, the fact that he perjured himself, under oath, when his perjury could have easily been documented, merely by looking at the paper he'd co-authored the year before, speaks volumes to his credibility, even under oath. And, since it is his credibility that is at issue here, my point is made.

I submit that either Gallo never did any such experiments, or more likely, that he did do such experiments, but never published the results, specifically because the data proved the opposite of what he claimed in his testimony.

Nor, to my (nor apparently Dr. Gallo's) knowledge, has any such experiment been done by anyone else, using co-culture or any other viral isolation technique. I have invited you, eagerly invited you, and now I'm openly begging you to prove me wrong about this.

There being no documented correlation between being HIV-antibody positive and actually having HIV, there is no basis for us to even speak of specificity or sensitivity of HIV tests, and therefore any claimed sensitivity or specificity is entirely without rational scientific basis.

In the early days of AIDS research, sensitivity and specificity were determined using not viral isolation or even co-culturing, but were purely based on the presence of AIDS-indicator illness or what the researchers judged to be "pre-AIDS" (which is about as meaningful as to say that a woman who is not pregnant is in "pre-pregnancy", since it assumes psychic ability to determine who will or won't develop AIDS in the future, at a time in which very little was known about AIDS,) combined with the subject being in a "risk group" (or not.) As I alluded to earlier, this is purely prejudice, based on circular logic, as those who are considered to be HIV-positive are assumed to be HIV-positive based on facts not in evidence, and in place of evidence prejudice becomes the determining factor as to who is or isn't considered to be truly infected.

More recently, HIV tests are "validated" by correlating them to previous tests. This is the basis for the claim that HIV tests have become more accurate over the years. In actuality, all it really tells us is that as HIV tests have become "more accurate", they are getting closer and closer to being 100% as accurate as previous tests that were less than 100% accurate -- a mathematical impossibility. Indeed, given that previous tests are said to be less accurate, a point would be reached beyond which increasing accuracy would result in less correlation to previous tests, not more. Heckle and Jeckle can agree 99.5% of the time, 99.9% of the time, or for that matter 100% of the time, but this still doesn't address the question of whether or not they're telling the truth, without corroboration.

Failing corroboration from an objective source (ie viral isolation), there is no basis to even make a wild guess at whether Heckle and Jeckle are telling the truth.

...And again, I'm down on my knees begging you, please prove me wrong, by showing me the literature on so much as a single HIV test, ELISA, WB, PCR, oral, or other, in which correlation was demonstrated using actual viral isolation (as opposed to specious and prejudiced circular logic) as a gold standard.

Failing that, you cannot bear your burden of proof by citing studies in which HIV seropositivity was correlated to AIDS, since there are more reasonable explanations for this correlation that do not violate the principle of least hypothesis, in that they do not postulate the existence of a shape-shifting virus that can only be detected using indirect surrogate markers. (Which is like saying that unicorns are invisible and can only be detected by searching the forest for their spoor.)

Jean-Marc wrote: "For cases such as these [infants], PCR or [RT-PCR] are usually used..."

Were you aware that the inventor of the PCR technique (Nobel laureate Dr. Kary Mullis) is a prominent AIDS dissident? Were you aware that he maintains that the PCR technique, as it is used in HIV viral load testing, constitutes fraud?

Maybe not. Were you aware that there is no PCR or RT-PCR test which does not come packaged with a disclaimer which states that the test is not to be used to diagnose HIV infection?

Maybe you weren't even aware of this, but were you aware that viral load has been estimated to represent anywhere between 99.99% and 99.9999% non-infectious particles? (Piatak M, Saag MS, Yang LC, et al. High levels of HIV-1 in plasma during all stages of infection determined by quantitative competitive PCR. (1993) Science: 259; 1749-1754)

Try the following experiment: Go to your doctor, and tell him that you want to get tested for HIV, but that you don't trust the ELISA and Western Blot tests, and that you want to get tested using a PCR or RT-PCR test. "After all, doc, if I don't have HIV, won't my viral load be zero?"

What he will tell you is that this is not the case. Indeed, cases have been documented of subjects with no infectious virus, who showed viral loads as high as 815,000 copies per milliliter (Piatak et al, Science 1993)

Furthermore, positive viral loads have been demonstrated in persons with no discernible risk, who were HIV-antibody negative using different screening tests, but 10%-20% of whom nonetheless were PCR-positive, using three different PCR tests, and more than half tested false-positive a second time, of those that were available to be re-tested. (Mendoza C, Holguin A, & Soriano V . False positives for HIV using commercial viral load quantification assays. (1998) AIDS; 12(15); 2076-2077)

In one case study, a patient was found to have repeated false-positive viral loads, ranging from 10,000 to 100,000 copies/ml, despite consistently testing antibody-negative over an extended period of time (Schwartz DH et al. Extensive evaluation of a seronegative participant in an HIV-1 vaccine trial as a result of a false positive PCR. (1997). Lancet: 350; 256-259) Because this patient was experiencing illness for at least part of this time, the possibility is suggested that false positive viral loads may well correlate to illness, rather than correlating to HIV itself.

Indeed, this suggestion is further supported, by another study which found false-positive viral loads up to 1.5 million copies/ml, in patients previously diagnosed with acute mononucleosis. (Rosenberg ES, Caliendo AM, Walker BD Acute HIV Infection among Patients Tested for Mononucleosis. (1999).New England Journal of Medicine; 340 (12):969)

Another study found that "The failure to demonstrate seroconversion... among those with positive PCR tests suggests that false positives occur even under stringent test conditions. The low predicitive value of a positive or indeterminate PCR test... contraindicates the routine use of gene amplification in this clinical setting." (Gerberding JL Incidence and prevalence of HIV, hepatitis B virus, and cytomegalovirus among health care personnel at risk for blood exposure: Final report from a longitudinal study. (1994). J Infect Dis 170; 1410-1417)

Indeed, in at least one case, false positive viral load was documented in a 5-month-old baby whose parents were both HIV-negative. (Mendoza et al 1998)

...So, you were saying about how these PCR-positive infants who developed AIDS proved that HIV causes AIDS? How do we know that these infants actually had HIV, and how do we know that their illnesses were actually AIDS?

(For more info on false-positive viral loads, click here. I don't know if this paper was ever published, but it is heavily referenced from the established medical literature.)

Jean-Marc wrote: "As a side note, nowadays most people in the US that show as positive on the ELISA are tested using a second method which can include PCR, and western blots"

I was aware of this. What I fail to see is how one non-specific test can confirm another. Is it possible to confirm the results of a coin flip by rolling dice?

Jean-Marc wrote: "To claim that these people had a 'plethora of antibodies which registered on the tests because they were sick…' indicates a belief that almost any antibody can cross react with this test. If this were the case..., quite frankly, EVERYONE would show up positive on the ELISA."

It's funny (hilarious, actually) that you should say that, since I know of one published article whose title is almost word-for-word, exactly that: Everybody Reacts Positive on the ELISA Test for HIV, R. Giraldo MD, Continuum, midwinter 1998/9

Dr. Giraldo describes how he has run ELISA HIV tests (including testing his own blood), on about 100 HIV-negative specimens, testing them first using the standard 1:400 dilution suggested by the manufacturer, and then subsequently running them using neat serum, finding that 100% of tests found to be HIV-negative at the standard dilution, show to be positive when the test is run undiluted.

Perhaps you would contend that it is unscientific to run an ELISA test in a manner inconsistent with its labeling. I would counter that what's unscientific is the use of dilution itself, combined with an arbitrary cutoff value, suggesting the rather unlikely premise that while everyone has HIV antibodies, only those with the most HIV antibodies actually have HIV.

Perhaps, also, you would contend that since Continuum is no longer in business, and since it was known for publishing articles contrary to mainstream views, that it is not a credible source. I would counter by inquiring why more financially successful journals (being kept that way by advertising dollars from pharmaceutical companies and others with vested interest), which studiously avoid publishing articles contrary to their advertisers' interests, should be considered any more credible.

At any rate, if you wish to prove your assertion that only those with HIV test positive on ELISA, you have a golden opportunity to prove your assertion by duplicating Dr. Giraldo's experiment, given that you "perform quite a few of these boring tests a week and know them like the backs of [your] hands." Since the burden of proof is upon you, you must prove this assertion or withdraw it, thus conceding my point that everyone has HIV antibodies, not only those who have ever been exposed to HIV.

Jean-Marc wrote: "SCID Mice Models and my attempt to explain in lay man’s terms why they are relevant to this issue..."

I must admit, once again, that I am as yet underqualified to hold my own in this particular discussion. However, given my intent to thoroughly study the literature you've sent on the subject, this will not be the case for the entirety of this debate.

Thus, I would like to request that we table this particular issue for now, while I get up to speed on it, and discuss the other issues that both of us have raised up to this point. Given the volume of this subject matter already on our plate, we should have plenty to discuss until such time as I've become more familiar with the animal studies you've mentioned.

In the meantime, if you can find the time, feel free to shoot me emails (separate from this discussion) giving your interpretations of the data presented in the studies you've sent, as this will no doubt accelerate the learning curve.

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

Jean-Marc wrote: "Mediation of apoptosis (programmed cell suicide) of UNINFECTED cells by GP120 (HIV envelope protein) (http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=446229&blobtype=pdf)"

OK. Having read the article, I am at a loss to see what it proves.

Now, I know that I'm probably wearing on your patience, and that you're probably convinced that I simply refuse to see that which I refuse to believe. Let me assure you that this is not the case. I am being difficult, but not merely for the sake of being difficult. It's just that I could cite reams and reams of cases from scientific history, of all sorts of concepts with no scientific validity, which were accepted by the mainstream scientific community, and about which volumes of articles were published in scientific literature. These include the existence of vampires, the idea that masturbation causes blindness, phrenology, the idea that feminine horniness is a disease, nuclear winter, the Y2K bug, "reefer madness", global cooling, and a long list of other things that have since been conclusively refuted, beyond the shadow of a whisker of even the most unreasonable doubt.

1) In the entire article, there is not a single instance of experimental evidence being presented. Presumably, the evidence may be found in one or more of the citations, but there being 168 of them, I am not about to spend the rest of the month trying to locate and read all 168 articles.

2) I am familiar with several (though admittedly not all) of the hypotheses contained in the article, but most if not all of these hypotheses are too new to have been scientifically tested; thus, none of them constitute proof of the basic facts we are trying to establish here. I am not like most laymen, in that I don't confuse the "latest breakthrough" with the truth. "New" and "true" may rhyme, but in science they very rarely correlate. Give me a tried-and-true hypothesis any day (or better yet, a theory that has stood the test of time and extensive scientific scrutiny.)

I must say that it is my own fault that we're getting so mired here, since I introduced an irrelevancy by way of mentioning the apparent lack of an explanation for the mechanism of HIV pathogenicity. This opened the door to other irrelevancies, and since that time, we've been leap-frogging past the basic proofs I've asked for, to correlations whose meaning has not been established in this debate, and further, to proposed hypothetical mechanisms which are as yet untested and therefore irrelevant to the very basic questions we are attempting to address here. In other words, we're getting WAAAY ahead of ourselves here.

Thus, I feel that in order to get the debate back on track, we must stick to a very specific, rigid chain of evidence and logic, on a step-by-step basis:

Step 1) Prove that HIV exists as a single, unique, exogenous retrovirus. Correlations between tests whose relevance has not yet been established in this debate, illnesses that may or may not be caused by HIV, and "risk groups" whose definition may be the result of specious and/or circular logic, do not constitute proof of this fundamental premise.

The proof of the pudding is in the eating, and the only acceptable proof of a virus is in the isolation of the virus itself. Only when this has been adequately established may we move on to Step 2.

Step 2) Prove that HIV is infectious.

This can only be done by culturing the virus in a previously uninfected host organism or cell culture. Unlike most dissidents, I am not particularly anal-retentive as to the specific method used, but I do insist on a few simple, basic criteria. A) The virus, in a reasonably purified form, must be inserted/injected into a previously-uninfected host or cell culture in a small amount; and B) After a suitable gestation period, it must be possible to harvest a larger amount than was originally inserted/injected into the host or culture, thus proving that the putative virus is capable of replication. Note that this sidesteps the usual dissident arguments concerning whether HIV is present in sufficient quantities to cause disease, or whether it lyses, since all we're looking for is whether or not it can reproduce, and we don't care how much it reproduces or how it reproduces, only that it does reproduce.

Now, given that you contend that HIV need not necessarily be present in large quantities, nor must it necessarily infect a cell in order to kill it (debatable, but admittedly not entirely inconceivable,) I nonetheless must insist that HIV be, at minimum, proven capable of replication, since if it isn't, then it wouldn't be able to sustain itself in the body, nor would it be able to produce viral copies for the purpose of spreading the infection to other hosts. If it cannot sustain itself and/or if it cannot spread from one host to the next, then there can be no infection, much less could there exist an epidemic.

Before moving to Step 3, I would like to pause for clarification of 1 and 2.

The Pasteur Institute set forth a set of criteria in 1973, for proving the existence of an infectious retrovirus. While it would be nice if these criteria were met, I do not insist absolutely that the Pasteur standards be adhered to, so long as the method in question can be shown to have been tested, and found to be A) Capable of success in a reasonable number of cases of putatively infected hosts, cells, cultures, or tissues (I don't insist that the method produce viral isolate every single time, as there are factors that might confound the attempt to culture and isolate it, which would not necessarily indicate that the virus was nonexistent or non-infectious); B) Incapable of producing virus from tissues, cells, cultures, or hosts where HIV could not possibly be present (I do insist that this criteria be met in 100% of cases, as even a single case of the magical appearance of a virus that wasn't supposed to be there casts serious if not fatal doubt on criteria A); and C) It must be reproducible.

Once steps 1 and 2 have been adequately addressed (and only then,) we can move on to Step 3.

Step 3) Establish that one or more HIV tests have been correlated to actual viral isolation, as established in Step 1, showing a high degree of specificity.

Now, at this point I would like to point out that I do not insist that the test be perfect, merely that it be reasonably accurate for the purpose of Step 4. To that end, sensitivity is irrelevant, as it doesn't matter whether we unwittingly eliminate false negatives; but conversely, specificity is of utmost importance, as Step 4 would only be confounded by the inclusion of an unacceptable number of false positives.

Step 4) Establish, using the test or tests which have been validated to the standards in Step 3, that AIDS-defining symptoms are substantially more prevalent in HIV-positives than among persons with no risk for HIV, after all other potential factors (lifestyle, drug abuse, malnutrition, etc.) have been controlled out.

Note that I do not insist that Koch's postulate's be met. I do not believe them to be relevant, for two reasons: 1) There will always be individuals who are immune or resistant to any given pathogenic microbe, therefore we should be more suprised if 100% of infected individuals developed the disease, than if not everyone did; and 2) As you pointed out, the same set of symptoms might be produced by other factors, thus even if there were HIV-negatives who developed disease indistinguishable from AIDS, this would not mean that HIV doesn't cause AIDS.

Given that the standards in Step 4 are a bit lax, one additional step must be added to remove all doubt that HIV causes AIDS.

Step 5) Prove that AIDS does not predate HIV infection.

This is important, in that we still haven't eliminated the possibility that HIV is a symptom of AIDS (ie merely another opportunistic infection), as opposed to being the cause. Dr. Gottlieb, the physician who documented the first 5 cases in 1981, was convinced that AIDS was caused by CMV, due to the fact that all 5 patients had current or prior CMV infection. It being more likely that CMV was a symptom of the disease rather than the cause, we cannot ignore this precedent, and therefore we must prove that AIDS does not cause HIV infection. Since an effect cannot predate its cause, proof that AIDS doesn't predate HIV infection would prove that HIV causes AIDS, and not the other way around.

----

NOTE: Lest we become confused about what the outcome of this debate does or doesn't prove, I should concede now that even if you fail to bear your burden of proof, this does not mean that HIV doesn't exist or that it doesn't cause AIDS, nor does it mean that such proof does not exist. At most, it would mean that neither you nor I can prove these things, and absence of proof does not constitute proof of absence.

However, as I've said earlier, if it proves that you are unable to satisfy your burden of proof, I would be more than glad to follow this debate up with one in which the burden of proof is upon me instead, to prove my assertion that this whole AIDS thing was a fraud from the get-go, without a shred of scientific validity.

Jean-Marc wrote: "Remember that the T-cell depletion is NOT a single-mechanism event!"

I hear ya, but the only difference, from my point of view, between a single-mechanism model of AIDS and a multi-mechanism model, is that multi-mechanism models are exponentially harder to disprove, and thus harder to put to the scientific test of disproof. According to Popperian scientific doctrine, this means that such a hypothesis is less scientific than a single-mechanism model, not more.

Of course, being unscientific doesn't mean that it has no objective validity. Once upon a time, there was no way to disprove the idea that other stars are orbited by planets, as ours is, and thus the idea of the existence of planets outside our solar system was unscientific. In the very recent past, however, this has changed, and in a relatively short time astronomers have documented evidence of literally hundreds of star systems in our galaxy, proving once and for all the objective validity of the concept of extrasolar planetary systems.

However, until such time as these new multi-mechanism hypotheses can be scientifically tested, they amount to no more than plausible speculation, and thus have no place in a discussion of what is or isn't proven.

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

Here is a link to a full length article in which the authors transfect HeLa cells with HIV proviral DNA to obtain infectious viral particles. The isolation and propagation is described starting on page 2 "Virus propagation and virus infection."

A few words on what may cause confusion in this paper as I'm not sure your level of knowledge on hybridomas and genetic manipulations.
1) HeLa cells are an immortal cell line derived from the cervical cancer induced by an HPV infection in a black woman back in the 1950s. These cells do NOT express CD4 and thus are not infectable by HIV (although some HeLa cells have been genetically altered to express it in some early experiments to determine which cell factors HIV required for cell entry. I'll look for this paper if I find time) The ones in this paper do not appear to be those cells but rather the CD4- cells. Also, during the propagation of HeLa cells, the HPV genome have been selected out and is no longer present. These are tested for on a genetic level (usually PCR). A Wikipedia entry on HeLa covers pretty much all anyone would want to know about them.

2) Transfection is a term for the introduction of DNA into a cell. This can be done (as in this paper) by addition of calcium chloride to DNA (which causes it to precipitate and stick to the cell surfaces). Cells can take in this naked DNA and then express the ORFs provided that the right requirements are present.

3) That said this paper provides evidence of (i.e. keep an eye out for the following as you read this paper)
a) Cell killing by HIV through direct cell killing
b) Formation of syncitia mediated by HIV
c) Isolation and propagation of HIV
d) The ability of HIV viruses generated from one cell line (HeLa) to infect CD4+ cells and produce another generation of particles.

4) While it would be tempting for one to point out that the donor (an asymptomatic hemophiliac) was asymptomatic due to the presence of HIV with lowered ability to kill T-cells, this is but a single isolate. Other normal cytotoxic HIV were also present but selected out (see section "Isolation of noncytopathic HIV-1 variants"). It is entirely possible that he was asymptomatic due to the amount of time since he was first infected.

Here is a second paper using the isolation and propagation of HIV particles.
and
Here a third paper documenting the transfection of several HIV proviral DNA sequences. This one is interesting because it uses a clone whose reverse transcriptase was mutated though selective stres using AZT.

Anyway, I have included these three papers as further evidence to the isolation of, infection with, and propagation of HIV viral particles by researchers. These cover quite a bit of info and I understand if it takes a bit of time to process these. Please let me know when you are done and if there is anything in there that requires clarification. (I gotta say I loved reading these three in particular because they dealt with genetic level fun!)
These should cover many objections presented in terms of isolation, infectivity, ect...
Don't hesitate to ask any questions you may have.
Cheers,
-Biolad

I must say, the Jackson study really impressed the hell out of me -- at first. For a minute there, I was almost convinced that I'd seen the Holy Grail -- that you'd sent me the study I'd been looking for for years, which proved that HIV existed, and that it was so strongly correlated to AIDS that it would be impossible to deny at least the strong possibility of a causal link. It was perfect!

...The more I thought about it, though, the more I realized, it was too perfect. So perfect, in fact, that it can't possibly be true.

The Jackson study is plainly corrupt, and was arguably done for the sole and specific purpose of discrediting Duesberg, who'd published his first dissident paper on AIDS only three years previously. Indeed, the very first and last paragraphs practically come right out and say as much.

Now, before you dismiss what I just said, hear me out, for I can prove conclusively that this is the case; for, you see, the researchers over-reached in order to make their case appear to be airtight, making impossible claims that defy rationality, and I am about to prove it mathematically.

Before I do so, though, a quick lesson from scientific history, which certainly applies here: "Real discoveries of phenomena contrary to all previous scientific experience are very rare, while fraud, fakery, foolishness, and error resulting from overenthusiasm and delusion are all too common." (Cromer 1993).

Quoting from the study: "We isolated HIV-1 or detected HIV-1 DNA sequences from the PBMC of all 409 [100%] HIV-1 antibody-positive individuals."

Did you spot the obvious lie? If not, don't feel too bad. I didn't either, at first. In fact, I was almost ready to concede this whole debate, on the strength of this one study.

Where are the false antibody-positives? Logic tells us that there should almost certainly be false positives in such a large group, and yet, there is no room for any false positives. Where are they? Are we to believe that the HIV antibody tests in use prior to 1987-1988 (when the study was actually conducted) were 100% specific?

In an earlier email, you said something to the effect that ELISA is not perfect, and anyone who says otherwise is a liar and/or a fool.

Now, at the risk of putting words in your mouth, I suspect that you would agree that the same goes for an algorithm of ELISA and WB (the standard cited by the study for seropositivity.) Even today, there are no credible claims that the ELISA/WB combination is 100% specific (as I pointed out earlier, there are claims to this effect in existence today, but these claims are supported by the comparison of the current tests against previous tests, which are widely acknowledged to have been less than 100% accurate. Thus, such claims are not credible, hence my choice of words.)

Given that the study was conducted in 1987-1988, using subjects that had presumably tested positive even earlier, what we're suggesting here is that the tests in use circa 1985 were 100% specific. Combine that with the current claim that HIV tests have gotten more accurate over the years, and what you have is one hell of an impossibility.

Just how specific were the tests in the mid-80s? Let's not bother with that question; for generosity's sake, I'm going to use as my primary figure, your highest claim to date for current tests of 99.92% specificity. (I will also use another example as well, being conservative in the extreme, for further generosity.)

Now, let's round that 409 figure to 400, just to make the numbers a little less awkward. I'm also going to be a bit lazy with the math, but I'm going to compensate for this by being so conservative in the end, that there can be no doubt that I have erred on the side of caution by a wide margin.

Given a seroprevalence in the US in the mid 1980s of 1:250 (1 million estimated infections / 250 million Americans), this group of approximately 400 HIV-positives can be extrapolated to a larger random sampling of approximately 100,000 people. Now, again, I'm being a bit lazy with the math, since it's rather time consuming to extrapolate exact figures, since we must assume that some of the 400 were false-positive, and therefore we can't count them as HIV-positives, but I will make up for this in a second.

100,000 - 400 = 99,600

The specificity gap (as I described in my earlier email) of a test with 99.92% specificity is .08%, or .0008.

99,600 * .0008 = 79.6, or approximately 80 false positives.

Now, to be conservative, let's just take a tenth of that figure, and assume that in a group of 409 seropositive individuals, only 8 were false positive. Would you agree that I'm being generously conservative here?

For that matter, let's say, just as a side example, that we use your logic from earlier, and assume an "accuracy" of 99.5%, and thus an "accuracy" gap of .005.

409 * .005 = 2.045, or approximately 2 false positives.

So, by estimates that are generously conservative in the extreme, we have to assume that a minimum of anywhere between 2 and 8 false-positives were among the 409 seropositive individuals.

Last time I checked, the term "false positive" meant that you don't have HIV, so how did they culture HIV from these 2-8 false positives?

In reality, all I needed was one false positive to cast doubt on the other 408, because if they cultured HIV from even one person who really didn't have HIV, then that makes for a pretty big question of what they were actually culturing from the others. If that one person didn't have HIV, then we can't assume that what was cultured in the others was actually HIV.

And having established that, it is fair to say that it most likely wasn't 2 false positives, nor was it 8. Given the relatively low specificity of HIV tests in the mid 1980s, 50 would be a conservative figure, 75 would be closer to what we might expect if HIV tests were as accurate then as they are claimed to be today, and arguably, there is a better-than-decent chance that the actual number of false positives was in excess of 100.

Now, at this point, I should point out that "isolation" in this study actually breaks down into two categories: Isolation by co-culture and "isolation" by PCR. PCR is not isolation, it is amplification (and not of the whole viral genome, but of only fractional particles, said to represent a tiny percentage of the whole HIV genome. This is why PCR "detects" HIV in people who don't have HIV.) In reality, isolation by co-culture was only successful in 98.3% of the 409 subjects.

Now, I would feel much better if this figure were lower, because we both know that isolation is not 100% successful, even in people we know to be infected with a particular virus. Sometimes, the culture simply fails, perhaps due to human error, or perhaps due to factors beyond even the most competent scientist's control. Thus, even if there were no false positives, it would not be unreasonable to accept a significantly lower success rate, and if the figure had been lower, I would have accepted that.

However, given that there must have been false positives, the figure is unacceptably high, since it implies that co-culture of HIV was successful even in persons who were false positive and therefore didn't have HIV. Given that 402 co-cultures were successful (98.3%), the remaining 7 are, admittedly, within our earlier 2-8 range, but it must be remembered that this was a deliberately conservative estimate, based on "accuracy" or specificity of what are claimed to be some of the most accurate tests available today, and divided by 10 to arrive at the upper limit of that range. The only way, in other words, that there were only 7 false positives in the entire group is if HIV tests available circa 1985 were 10 times more accurate than they are today. Since we both know this is not the case, there's a hole in this study that you could drive a herd of elephants through.

These researchers got greedy, plain and simple. They were like the kid that got caught changing the grades on his report card, because he'd changed all his F's into A+'s, when it would have been easier and far more believable to have forged B's instead.

There are other things about this study that don't quite pass the smell test, but given this one whopper of hole I just found below the waterline, to discuss them at this point would be like shooting a BB gun at a sunken ship.

In conclusion, the article states: "In summary, we were able to definitively demonstrate that HIV-1 infection is present in all HIV-1 antibody-positive adults, regardless of clinical status, by using a sensitive culture or PCR assay for detection of the virus. Certainly the argument that HIV-1 is not the cause of AIDS because it is not present in all HIV-1-seropositive AIDS patients is no longer tenable."

This, and the very first sentence, ("The role of human immunodeficiency virus type 1 (HIV-1)as the cause of the acquired immunodeficiency syndrome (AIDS) has been challenged because HIV-1 was not isolated from 6 to 50% of HIV-1-seropositive AIDS cases reported,") expose the true motivations behind this study. If you'll check the citations (4,5), what you'll find is that this study was intended to serve the sole and specific purpose of discrediting Duesberg.

Given other statements in this study, one is left with the impression that attempts at isolation prior to this had all had extremely low success rates (20%-42%), or otherwise had been successful in 100% of cases (which as I said earlier, is extremely suspect in that it assumes 100% specificity for HIV tests circa 1985.)

Since any study claiming 100% specificity for HIV tests can only have been authored by, in your own words, fools or liars, (particularly in 1990), we can only assume that those studies which produced the lower success rates are the more believable of the lot, and we are still left wanting for a single study which credibly establishes a high enough degree of specificity for HIV tests, to suggest that they correlate to actual infection, rather than to disease and/or so-called "risk factors".

Bottom line: The only thing this study proves is the existence of AIDS researchers without scruples. I already knew that those existed.

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

Also a concluding comment on your comment about the Jackson paper.

Was this a paper "direct attack on Duesberg"? No. It was however a direct challenge to his claim. If you read the first papers I sent you "Kochs_postulate.pdf" you will see Duesberg made a big claim by saying that HIV couldn't be the cause of AIDS because HIV was only present in a small number of AIDS patients. At this point he was not referring to false positives but to what was later found to be false NEGATIVES. His assertions of less than 50% presence of HIV were based on the initial and less sensitive methods of testing which have long ago refuted this (also in Kochs_postulate.pdf). The HUGE difference here is that the lowered sensitivity of the methods gave false NEGATIVES. This paper used more updated and sensitive techniques to show that HIV is in fact present in all AIDS patients.

Just a side note on one of the later comments you made.
Cheers,
-BioLad

Jean-Marc wrote: "To say the HIV test is 99.5% correct does not mean that you MUST have 1 error for every two hundred people tested every time it is run."

I am well aware of this.

Jean-Marc wrote: "n (sample population size) = 409"

Wrong sample size, due to what is obviously a gross misunderstanding of the concepts involved, but I'll get to that in a minute.

Jean-Marc wrote: "Statistically, with 409 samples and an accuracy rate of 99.5% one would expect that 409*0.995 are correct."

And here's that gross misunderstanding I was referring to.

Where do you get the idea that the term "accuracy" is ever used in this context, by anyone but laymen? Indeed, the term "accuracy" is utterly inadequate to describe the accuracy parameters of a binary test which might return both false-positives and false-negatives.

The correct terms (and I can't believe I'm having this discussion with a man who has a Master's in biology and who is entrusted with the responsibility of running tests that may mean a patient's life or death,) are sensitivity and specificity.

Now, it is true to say that if the sensitivity were 99.5% and we tested 400 people who were all HIV-positive, we'd expect, on average, 2 of them to be false-negatives.

However, the number of false-positives that would result from a test with 99.5% specificity cannot be calculated unless we first know how many HIV-negatives there are in the sample. (See Wiki article on specificity linked above.) Specificity is defined as the ability to correctly identify a negative condition, and the remainder are your false-positives. Thus, the number of positives is irrelevant to the issue of specificity, and therefore it is fallacious for you to attempt to use the 409 HIV-positives to determine how many might have been false positives.

And again, I am simply appalled that a man who doesn't understand these basic concepts is allowed to run ELISA tests. Perhaps in addition to having a degree in biology, you should study mathematics as well, and quit relying on a calculator, since a calculator in the hands of a man who doesn't understand the math is like an automobile in the hands of a man who doesn't know how to drive -- the best he can hope for is that he won't do anything fatal.

You made reference earlier to the Dunning-Kruger effect, and at the time, I suggested that the accusation might reveal more about the accuser than the accused. Now I'm not just suggesting it, I'm saying it out loud. So quit using your sheepskin to blow your nose, and go study the concepts of sensitivity, specificity, and Bayesian conditional probability, so that in the future, you'll be qualified to refute a high school dropout such as myself.

Jean-Marc wrote: "This does NOT however say that 2.045 false positives MUST be present."

No, it doesn't. But it is equally likely for there to be 4.09 false positives as for there to be none. (Assuming, of course, you were applying the mathematics correctly, which as I've already demostrated, you aren't.)

Jean-Marc wrote: "They only considered a result positive if it showed positive for the HIV p24 protein TWICE over the course of the incubation "

I don't care how many times they tested positive for P24. P24 is NOT HIV, nor is it specific to HIV.

43% of dogs test positive for P24. (Studies with Canine Sera that Contain Antibodies Which Recognize Human Immunodeficiency Virus Structural Proteins, Strandstrom et al, Cancer Research [suppl] Sept 1 1990. See attachment) Are you about to claim that nearly half of all dogs have Human Immunodeficiency Virus?

"At present there is ample evidence that antibodies which react with p24 are ubiquitous in both human and animal sera, which can only be interpreted that either p24, the antibodies, or both, are non-HIV-specific or a significant proportion of both humans and animals are infected with HIV." (The Isolation of HIV -- Has it Really Been Achieved? The Case Against, Papadopulos-Eleopulos et al, Continuum Sept/Oct 1996)

30% of people infused with blood containing no HIV test positive for P24. (What do Western Blot indeterminate patterns for Human Immunodeficiency Virus mean in EIA-negative blood donors?, Genesca et al, Lancet 1989)

"The presence of p24 band was common among low-risk, uninfected volunteers and complicated the interpretation of the Western blot test results." (Interpreting HIV serodiagnostic test results in the 1990s: social risks of HIV vaccine studies in uninfected volunteers, Belshe et al Annals of Internal Medicine 1994)

In another study, 82% of "presumably uninfected but serologically indeterminate individuals and 5/5 [100%] seronegative blood donors were found positive for p24." (False-positive HIV-1 virus cultures using whole blood, Schupbach et al AIDS 1992)

So I don't care how many times in a row these people tested positive for P24. As you yourself pointed out, it's possible to flip a coin 5 times and have it land on heads every time (probability 1:32), that doesn't mean that a coin toss is meaningful. Nor, unfortunately for you, is the finding of P24; twice, five times, or a hundred times. If a result is meaningless once, it's meaningless a thousand times.

Jean-Marc wrote: "HIV ELISA, at least the older ELISAs in use back when this paper was written, had a much higher rate of false positives for one specific group of people."

Let's not forget who else tests false positive for HIV antibodies:

Lepers (Leprosy as a cause of false-positive results in serological assays for the detection of antibodies to HIV-1, Andrade et al, International Journal of Leprosy, 1991; Infection with human immunodeficiency virus type 1 (HIV-1) and human T-cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabionomanna; Kashala et al, International Journal of Leprosy, 1994)

Persons with tuberculosis or mycobaterium avium (Kashala et al, International Journal of Leprosy, 1994)

Persons with systemic lupus erythematosis (False positive results for antibody to HIV in two men with systemic lupus erythematosus, Esteva et al, Annals of Rheumatoid Diseases, 1992; False positive tests for HIV in a woman with lupus and renal failure, Jindal et al NEJM, 1993)

Persons with flu (Serological diagnosis with recombinant peptides/proteins, Ng V., Clin Chem 1991)

Persons vaccinated for flu (Donor follow up of influenza vaccine-related multiple viral enzyme immunoassay reactivity, Arnold et al, Vox Sanguinis, 1994; Review of testing for human immunodeficiency virus, Bylund et al, Clin Lab Med, 1992; Pitfalls in HIV testing, Cordes et al, Postgraduate Medicine, 1995; False-positive ELISA for human immunodeficiency virus after influenza vaccination, Hisa J., Journal of Infectious Diseases, 1993; Laboratory diagnosis of human immunodeficiency virus infectionI, Proffitt et al, Inf Dis Clin North Am, 1993)

Persons with Herpes Simplex I or II (Identification of cross-reactive epitopes recognized by HIV-1 false-positive sera, Langedijk et al, AIDS, 1992; False-positive human immunodeficiency virus type 1 ELISA results in low-risk subjects, Challakere et al, West J Med, 1993; respectively)

Persons with upper respiratory tract infection, recent viral infection, or exposure to viral vaccines (Challakere et al, West J Med, 1993)

Persons with malaria (ELISA HTLV retrovirus antibody reactivity associated with malaria and immune complexes in healthy Africans, Biggar et al, Lancet, 1985; HIV infection and malaria, Charmot et al, Revue du Practicien, 1990)

...at this point, I'm getting tired of typing all these references, and I'm only a tiny fraction of the way down the list of persons who have been documented to test false positive on ELISA, WB, and/or PCR, so I'll refer you to a referenced list of factors known to cause false positives on HIV tests. Suffice to say, false positives in pregnant women is but the tip of the iceberg. Thus your argument is specious, in that it assumes that only pregnant women will test false positive, when it is plain that the facts are otherwise.

Jean-Marc wrote: "Another VERY important thing to notice here is that NONE of the HIV- sera produced p24..."

You're right -- that IS important. VERY important.

Considering, as I pointed out earlier, that P24 can be found in nearly half of all dogs, and up to 100% of uninfected humans (references already provided), it is more than a little suspicious that they couldn't find P24 in a single uninfected subject.

And why was the control arm of the study so small? We're talking about only 20 people here, in a study that included 409 HIV-positives. In a nation where HIV-negatives outnumber HIV-positives by a factor of 250:1, they couldn't come up with more than 20 HIV-negatives to include in their study?!

Do I detect a faint whiff of selection bias? No, that is no faint whiff, this reeks to high heaven. I cannot conclusively prove selection bias, since the authors mention not a single word of how or where they dug up these 20 HIV-negatives, but the suspicion is far too strong to be ignored.

Jean-Marc wrote: "...if you have non-anecdotal references showing false positives on the PCR I would be interested to see them..."

You've already seen them, provided you read my earlier email. However, I will repeat them here.

(Copied from my earlier email)

10%-20% is ridiculously small??? (Mendoza et al 1998, cited above) What would you consider statistically significant?

According to Gerberding JL 1994 (also cited above), the only thing ridiculously small is the predictive value of a positive or indeterminate PCR test, "even under stringent test conditions."

Jean-Marc wrote: "Those points being made I must assert that you may keep your holy grail."

You are mistaken. That was no holy grail. That was the Gosman taking the shot from downtown, and it was "Swish! 3 Points! Nothin' but net!" You just got schooled by a guy with a GED, and there's nothing for you to do but to be a gracious loser and take it like a man.

Don't take it hard, though. I myself used to think I knew far more about HIV than I really did (back when I actually believed in HIV,) and you are to be commended for your bravery in seeking out this debate, as the world's foremost HIV researchers have openly stated that they will not debate a PhD like Dr. Duesberg, or even some self-educated lowlife like myself, using the excuse that to debate us would only lend us credibility.

Which begs the question: How could we gain credibility in a fair debate, unless we won it fair and square? Food for thought.

--- Gos

--- gos@nerosopeningact.com

"I must confess my worst fault: Although I am a gracious loser, I am an insufferable winner. My apologies to those with swollen toes to show for it."

Gos,

Thank you again for pointing out my error on the issue of specificity and sensitivity. It forced me to look back and relearn it and has been very helpful and educational. I have finished re-reading your response to the Jackson paper. Here are my thoughts on it. For the sake of calculations I will use figures found in this paper on the sensitivity and specificity of ELISA and WB in 1988 and 1989 (I didn't see any concrete figures for 1987 but this paper gives lower specificity than my earlier figures of 99.5 so I figure it should be fair). Feel free to correct my math; I'm not claiming to be perfect. This paper specifies the following figures which I will use:

ELISA

Sensitivity: 99.7% (6545 of 6566 positives detected)

Specificity: 98.5% (3004 of 3051 negatives correct))

WB

Sensitivity: 99.3% (1345 of 1355 positives detected)

Specificity: 91.6% (306 of 334 negatives correct))

So here goes:

Presuming that our 409 samples were randomly taken from HIV+ detected people, out of 409 samples detected positive based on ELISA alone, 402.865 (409*0.985, rounding up for the sake of simplicity to 403) are expected to be true positives. This allows for 6 of the 409 to be false positives.

These are then tested by WB (which tests detecting different antigens), which in 1988ish had an average specificity of 91.6. Thus of the 6 expected to be false positives, 5.496 (6*0.916, we¢ll round down to 5) would be expected to be true positives as detected by the WB. This leaves us with 1 possible false positive.

However, this is presuming that the samples are taken at random from sera determined to be HIV+ by ELISA and nothing else yet. This was not the case. Of the 409 sera, 144 of them came from people with classic symptoms of AIDS or ARC. If we assume for the sake of argument (I know assumption is a dangerous thing) that HIV is in fact the cause of AIDS, then these samples are not random but expected to all be true positives. This leaves us with a randomly HIV+ determined group of 256 (asymptomatic patients). Following this group, of the 256 asymptomatic patients, 252.16 (round to 252 for simplicity) are expected to be true positives, leaving 4 possible false positives. Testing these by WB, we would expect that 3.664 (round up to 4) would be true. Thus, the Jackson paper is not at all impossible (I know you didn¢t claim it was) and also not improbable.

Let me know what you think. Like I said, I am not claiming to be perfect and notification of any errors would be appreciated.

Cheers,

-BioLad

(P.S. you had also mentioned in your first response that PCR detects HIV in people who are truly negative. Can you cite this? The papers I have seen do not agree with this and I would be interested in reading your source.)

Jean-Marc wrote: "Presuming that our 409 samples were randomly taken from HIV+ detected people, out of 409 samples detected positive based on ELISA alone, 402.865 (409*0.985, rounding up for the sake of simplicity to 403) are expected to be true positives. This allows for 6 of the 409 to be false positives.

These are then tested by WB (which tests detecting different antigens), which in 1988ish had an average specificity of 91.6. Thus of the 6 expected to be false positives, 5.496 (6*0.916, we¢ll round down to 5) would be expected to be true positives as detected by the WB. This leaves us with 1 possible false positive."

Jean-Marc wrote: "you had also mentioned in your first response that PCR detects HIV in people who are truly negative. Can you cite this? The papers I have seen do not agree with this and I would be interested in reading your source."

In order to answer that question, first we must define "truly negative", since the phrase could mean antibody-negative, having no infectious virus, having no HIV risk, or any number of other things.

In patients with no discernible infectious virus, viral load as high as 815,000 copies per ml were measured. (Piatak M, Saag MS, Yang LC, et al. High levels of HIV-1 in plasma during all stages of infection determined by quantitative competitive PCR. (1993) Science: 259; 1749-1754)

In another study, false positive viral loads were documented on three different PCR tests, in 10%-20% persons who were antibody-negative on several different tests, and who had no discernible risk. Of those available to be re-tested, more than half showed up false-PCR-positive a second time. (Mendoza C, Holguin A, & Soriano V . False positives for HIV using commercial viral load quantification assays. (1998) AIDS; 12(15); 2076-2077) The Mendoza article furthermore goes on to document a case of a false-positive PCR test in a 5-month-old infant whose parents both turned out to be HIV-negative.

In one case study, a patient was found to have repeated false-positive viral loads, ranging from 10,000 to 100,000 copies/ml, despite consistently testing antibody-negative over an extended period of time (Schwartz DH et al. Extensive evaluation of a seronegative participant in an HIV-1 vaccine trial as a result of a false positive PCR. (1997). Lancet: 350; 256-259)

Another study found mononucleosis to be linked to false-positive viral loads as high as 1.5 million copies per ml, in antibody-negative subjects. (Rosenberg ES, Caliendo AM, Walker BD Acute HIV Infection among Patients Tested for Mononucleosis. (1999).New England Journal of Medicine; 340 (12):969)

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

Here's an interview that touches on the topic of alleged "EM pics" of "purified" HIV.

mms://68.251.204.5/video/intimetv/ote003.wmv

--- Gos

Jean-Marc,

OK, then if what you're telling me includes all the relevant details, then I understood the RT paper better than I thought. However, before moving on to the RT paper, I want to address the Brandt paper, as I promised I would in an earlier email.

First, however, I want to go back to the Jackson paper, because much of what I have to say about Brandt is set up in Jackson.

Earlier, you said that I'd been uncivil in my characterization of Jackson as fraudulent. I would counter by saying that if my 10-year-old daughter drove up in a brand new Lamborghini and told me that she'd purchased it with the money in her savings account, I would openly accuse her of something shady, and it would not be considered uncivil, for I could be virtually certain that she did not come by it honestly.

You also said that I'd accused the Jackson researchers of "attacking" Duesberg. I never used the word "attack"; the word I used was "discredit", and there's nothing wrong with a scientist setting out to discredit the arguments of another scientist -- it's how science is done. I personally believe Duesberg to be discredited on several counts, though I'd say that a good 90%-99% of what he says is spot-on. I certainly do not idolize Duesberg to the point that I would consider it an "attack" for other scientists to attempt to pick apart what he's saying.

However, there is one little thing: They have to come by it honestly, and Jackson et al could not possibly have come honestly by the results they reported. I have a better chance of believing my daughter will drive up in a new Italian sports car that she'd gotten for less than the $170 she's got in her savings. As I demonstrated earlier, there should have been nearly 100 false-positives in a group of 409 ELISA/WB HIV-positives, and one should almost certainly expect dozens of false positives at the very least in a group that size, given the sensitivity and specificity you quoted for ELISA and WB circa 1987. The very best that Jackson offers is 7 HIV-positives in which they couldn't directly co-culture HIV, but for whom they were able to obtain positive PCRs. However, if we assume that those 7 were in fact false positives, then that means that Jackson documents 7 cases of PCR false positives in false-ELISA and false-Western Blot positives. And if we assume that those 7 were our false positives, that still doesn't come close to the number of false positives that we would expect to see, and the odds against it are still astronomical.

Now, as to whether this article was published in response to Duesberg and no other, allow me to quote from the very first sentence of the paper: "The role of human immunodeficiency virus type 1 (HIV-1) as the cause of the acquired immunodeficiency syndrome (AIDS) has been challenged (4, 5) because HIV-1 was not isolated from 6 to 50% of HIV-1-seropositive AIDS cases reported..." Now, if you look at citations 4 and 5, you'll see that this is in reference to two Duesberg articles [(4.) Duesberg, P. 1988. HIV is not the cause of AIDS. Science 241:514-517. (5.) Duesberg, P. H. 1987. Retroviruses as carcinogens and pathogens: expectations and reality. Cancer Res. 47:1199-1220.] In addition, the Jackson study commenced in 1987, the same year Duesberg published Retroviruses as carcinogens and pathogens: expectations and reality. Coincidence? Maybe, maybe not. Given the very first sentence of the article, I'd say that it was probably no coincidence at all. This paper was published for the specific purpose of addressing (or at least appearing to address) one of Duesberg's challenges.

And again, there's nothing wrong with that, IF you come by it honestly. According to my calculations, the odds are in the millions of trillions of trillions of trillions to one that they could not possibly have honestly come by the results they claimed. In their zeal to discredit Duesberg, they over-reached and claimed the impossible: That 100% of ELISA- and Western Blot HIV-positives had culturable virus, even though the laws of statistics dictate that there should have been about 98 false-positives in a group of 409 ELISA- and WB-positives who should not have had any culturable virus. This is where science stops being science, and is appropriately referred to with the ugly word "fraud", and there's nothing uncivil about saying it out loud.

The Brandt study suffers from the same fatal flaw as Jackson, in that it could only be valid if we are to assume that ELISA and WB tests pre-1992 were 100% specific to HIV, which we both know that they weren't. However, because the study included fewer than 1/3rd of the HIV-positives in the Jackson study, the odds against there being no false positives are a bit better, though still astronomical. On the flip side of the same coin, however, the Brandt study being smaller than the Jackson study stands as much against it as in its favor, since smaller studies tend to have far higher statistical noise floors to begin with.

A far more interesting angle on the Brandt study is what it reveals in terms of "scientific" practice common to most or all HIV/AIDS research. Quite frankly, both in terms of scientific research and the diagnoses and treatment of individual patients, HIV "science" is riddled with selection bias, confirmation bias, and other forms of specious reasoning. The authors of the Jackson study did not go into a great deal of detail on their methods of selection of subjects, but the Brandt study is a bit more detailed in this regard, and what it reveals is somewhat shocking.

First, the criteria for selection are set forth: The patient was considered infected if HIV antibodies (as "confirmed" by ELISA and WB,) persist beyond the age of 15 to 18 months, OR HIV was co-cultured from their blood (a total of 6 patients out of nearly 200 in the study,) OR they met the 1987 CDC case definition for AIDS (a definition which included persons with no laboratory evidence of HIV infection in the absence of other known causes for immunosuppression.) On the flip side, subjects were considered uninfected if they were well AND if they'd lost their maternal HIV antibodies (or never had them by virtue of having been born to an HIV-negative mother.)

This may look innocuous enough on the surface, until you consider the full ramifications of it. What's being done here is that groups of subjects are being broken down by "risk group" and/or "AIDS-indicator" illness and/or "HIV antibodies", and their HIV status is thus presumed based on these criteria (and given that some were likely considered HIV-positive in the absence of laboratory evidence of actual infection under the 1987 CDC case definition of AIDS, it may well be that a significant number were HIV-negative according to ELISA and WB.)

Then, the article goes on to say that those who were considered seropositive were sampled at 3-month intervals, more frequently if they were ill. Once again, we see a pattern of practice that is ubiquitous, not only in AIDS research, but at the patient-doctor level as well, of selectively testing and re-testing those considered to be "at risk" or "HIV-positive", without doing any such rigorous testing of those considered to be "low risk" or "HIV-negative". The inclusion of HIV-negatives in this study thus only serves to render the illusion that it is a controlled study, when in reality, if it were, the HIV-negatives would have been sampled every three months (or even more frequently,) just as the HIV-positives were, and that data would be presented.

The study further goes on to say that in several cases where they couldn't get a PCR reading on the first try, they re-tested the subjects, and in about half of those, got a PCR positive. Again, when the test tells us something other than what we expect to see, we repeat it until we get the results we expected. This is, by definition, confirmation bias.

Thus, while it is apparent that the study shows a correlation between the PCR tests and being seropositive and/or having illness, it is not readily evident whether this is because there's a virus at work, or merely an illusion created by selection bias and confirmation bias. If there were no real correlation to be measured, this would make it appear that a correlation existed, and if there were some correlation, this method would make that correlation appear to be virtually absolute even if it were not.

Personally, I think that there is some correlation between what is called "AIDS" and the antibodies, antigens, and protein fragments measured by the ELISA, Western Blot, and PCR tests, I'm just not yet convinced that the common thread is actually a virus, and neither the Jackson nor the Brandt study is nearly as compelling as might appear on the surface (a phenomenon I've observed throughout the field of HIV/AIDS research.)

Which brings us to the RT study. Before I comment on it, however, I want to re-read it, in light of the clarifications you've made about it.

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

OK, back to the debate...

Before I comment on the RT paper, let me make sure I've got the specifics straight:

1)  Particles were produced using the common co-culture technique used for HIV, which consists essentially of co-culturing putatively infected cells with special leukemia cells from an immortal line, and then shocking them with chemicals, thus producing particles which are referred to as "HIV virions".  Correct so far?

(Note on "Gallo's" cells:  Earlier, in a sidebar, you pointed out that I really didn't know for sure that Gallo had invented the cells used in the co-culture technique.  Upon further research, it turns out that I was wrong -- Gallo didn't invent this cell line, he borrowed it from its inventor; however, because he did so without attribution, a common misconception has arisen that Gallo invented this cell line.)

2)  Electron micrography was used to count the particles.

3)  Reverse transcriptase activity was measured, which was then correlated to the EM count produced in step 2, showing that the more particles were present, the greater amount of RT activity was found.

...Do I have the essence of the article down?  Are there any details I'm missing, and/or do I appear to have misunderstood any specific points?

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

Jean-Marc wrote:  "I was looking at your log of our conversations so far on your site and I think there is something wrong on my end.  I saw some comments you made recently that didn't seem to make it to my in-box.  If I miss an e-mail this is probably the reason although I can't say why it would do this since I get others from you just fine."

My guess would be that Yahoo's spam filters are sending some of the emails to your bulk folder -- happens to me all the time.  I recommend checking your BM folder frequently, using the "Not Spam" button to move legitimate emails to your inbox, and then deleting all the spam.

The conversation at the site is outdated as hell -- I've got an updated version on my local machine, but I'm still working on it (proofreading, checking HTML, etc.) and haven't uploaded it yet.  It's much better than the one that's up now, though, because I've reorganized the discussion, by separating out the main debate and putting all the sidebars on their own pages, so that they do not distract from the main body of the debate.  It reads much more fluidly now.

And speaking of which, it's about time for that first installment on the RT paper, so without further ado....

Jean-Marc wrote:  "One thing I would ask when you look into the procedures used is that you examine which chemical was used to 'shock' the cells and determine why/if it was needed in order to propagate the virus (by you doing so I am in no way assuming that you would acknowledge the existence of said virus or identify it as the cause of AIDS).  I think this may be helpful for the purpose of the understanding of this paper."

I must admit, that this is the hurdle that has kept me agnostic on the existence issue.  If I had better understanding of the process at the molecular level, I'd be better equipped to determine whether HIV exists in objective reality.

There is a somewhat famous debate that occurred between Dr. Duesberg and a group of Australian physicians on the existence issue, when Duesberg attempted to claim the Continuum Award for proof of the existence of HIV.  (Duesberg claims award; Perth Group reply; Duesberg response to PG; PG second reply)  I read the debate, but I have to admit that it got way over my head at some points.

However, I did understand enough of it to understand two things:

1)  "Retroviral" particles do not necessarily indicate viral infection, since they may not be infectious.

In 1972, Drs. Temin and Baltimore showed that the finding of particles with morphology consistent with retroviruses does not necessarily prove that they are retroviruses, even if they band at the 1.16 gm/ml density gradient.  (Temin HM, Baltimore D. RNA-Directed DNA Synthesis and RNA Tumor Viruses. Adv Vir Res 1972;17:129-186)

In 1976, another famous scientist said, famously, that in leukaemic cell cultures, "virus-like particles morphologically and biochemically resembling type-C virus but apparently lacking the ability to replicate [and therefore non-infectious and therefore non-viral], have been frequently observed." [bracketed comment mine]  (I'll leave you to guess, for the moment, who that scientist was.)

In the years 1975-79, another researcher showed retroviruslike particles to be found in milk, embryonic tissues, and the vast majority, if not all human placentas.  (Panem S, Prochownik EV, Reale FR, et al. Isolation of Type C Virions from a Normal Human Fibroblast Strain. Science 1975;189:297-299. ; Panem S, Prochownik EV, Knish WM, Kirsten WH. Cell Generation and Type-C Virus Expression in the Human Embryonic Cell Strain HEL-12. J Gen Virol 1977;35:487-495. ; Panem S. C Type Virus Expression in the Placenta. Curr Top Pathol 1979;66:175-189.)

In 1988, another group of researchers found "HIV particles" in 90% (18/20) of patients with generalized lymphoadenopathy attributed to HIV, but they also found the same particles in 87% (13/15) of patients with non-HIV lymphoadenopathy.  (O'Hara CJ, Groopmen JE, Federman M. The Ultrastructural and Immunohistochemical Demonstration of Viral Particles in Lymph Nodes from Human Immunodeficiency Virus-Related Lymphadenopathy Syndromes. Hum Pathol 1988;19:545.)  From this, the researchers were forced to conclude, "The presence of such particles do not, by themselves indicate infection with HIV."

2)  Reverse Transcriptase (RT) is not unique to retroviruses.  (Weiss R,Teich N, Varmus H, Coffin J. RNA Tumor Viruses. Cold Spring Harbor Laboratory. Cold Spring Harbor, New York;1982)

According to the famous scientist quoted above (have you guessed his identity yet?), RT can be found in Leukaemic T-cell lines (the immortal cell line used in HIV co-culturing is, in fact, a Leukaemic cell line.)  This same scientist was the first, in 1973, to demonstrate that RT can be found in "PHA stimulated (but not unstimulated) normal human blood lymphocytes."

According to a paper published in 1978 by another group of researchers, RT can be found in normal spermatozoa.  (Whitkin SS, Higgins PJ, Bendich A. Inhibition of reverse transcriptase and human sperm DNA polymerase by anti-sperm antibodies. Clin Exp Immunol 1978;33:244-251)

In 1987, Nobel laureate Dr. Harold Varmus found RT activity in normal, uninfected cells of yeasts, insects, and mammals.  (Varmus H. Reverse Transcription Sci Am 1987;257:48-54)

All of this, collectively, demonstrates that retroviruslike particles and RT activity are neither singly, nor by extension collectively, specific to retroviruses in general, much less to a given retrovirus.

By the way, have you guessed the identity of our mystery scientist?  It was none other than Dr. Robert Charles Gallo.  The quotes attributed to him can be found in the following articles:  Gallo RC, Wong-Staal F, Reitz M, et al. Some Evidence For Infectious Type-C Virus in Humans. In: Baltimore D, Huang AS, Fox CF, eds. Animal Virology. New York: Academic Press Inc.,1976:385-407;  Gallo RC, Sarin PS, Wu AM. On the nature of the Nucleic Acids and RNA Dependent DNA Polymerase from RNA Tumor Viruses and Human Cells. In: Silvestri LG, ed. Possible Episomes in Eukaryotes. Amsterdam: North-Holland Publishing Company, 1973:13-34.

----

At this point, we find ourselves in a quandary:  Thus far, no single piece of evidence you have put forth has conclusively proven the existence of HIV, and at this point in the discussion it seems likely that we're starting to get in a bit over my head, which makes it likely that further discussion would prove unproductive.

We also find ourselves still debating the existence of HIV after a month of debating, and no closer to proving one way or the other whether it exists.  This has kept us from moving on to other areas of debate.

For the sake of the argument, I shall thus concede the existence issue; not because I'm convinced that HIV exists, but because I'm not convinced that it doesn't exist, and I must concede, at the very least, the possibility that the proof, if it exists and is valid, may be beyond my current comprehension.  I must also concede the possibility that, while no single proof you've offered has conclusively proven its existence, it still may be that collectively, all of the phenomena you've documented point to a retroviral phenomenon.

And having thus dispensed with the existence issue for the purpose of this debate, only one question remains concerning its existence:  How do we know that it's exogenous, rather than endogenous?  Every cell in your body is loaded with enough retroviral code to build hundreds of retroviruses the size of HIV, and you inherited most or all of them from one or both of your parents.  Estimates on what percentage of the average person's genome is made up of retroviruses range from 3% to 8%.  Most or all of them are harmless, some appear to be symbiotic.

Indeed, because of the unique reproductive process of retroviruses, they tend to be dependent upon the host's continued replication for their own reproduction and survival, and this is why they were considered to be a candidate for cancer-causing viruses as early as the 1960s.

The question, therefore, becomes:  "How do we know that HIV is any different?"  How do we know that it is not endogenous and harmless, as Duesberg claims, even if we reject the Perthian argument that it's never been proven to exist?

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

Kewl.  While you're doing so, there's one other thing I forgot to mention in my previous email, that you may want to keep in mind as you're putting together your response.  I mentioned the question of whether HIV was exogenous, but skipped whether it is a single virus as opposed to multiple retrovirii -- needless to say, it can be a retroviral phenomenon without being a single virus, and so this question will be raised as well, as we begin to tie up the last loose ends of the existence issue.

--- Gos

P.S.  For some reason, Yahoo sent this email to my spam folder and your other email to my inbox, even though they're from the same address and I can see no significant difference between the two -- it does it to me all the time.  Fortunately, I keep my spam folder empty and check it regularly.

Jean-Marc,

The one place where I know for a fact that Duesberg makes the case for HIV as an endogenous retrovirus is in his book, Inventing the AIDS Virus, where he presents (among many other things,) his case that:

1)  HIV is not a new virus, it is an old virus.

2)  HIV is not exogenous and typically not contagious, being rather transmitted from mother to child as part of the human genome (ie an endogenous retrovirus).

I was able to find one article where he makes at least part of that particular argument, if not all of it:  AIDS Acquired by Drug Consumption and Other Noncontagious Risk Factors.  See Section 3.5.2:  HIV-Assumed to be Sexually Transmitted-Depends on Perinatal Transmission for Survival

As to the question of proving a negative, while it is true that a negative cannot be universally proven, science, (where actually practiced,) gives us an alternative:  Studies with large control groups, showing that HIV cannot be found among those with no conventional risk of HIV acquisition, using the same methods that are used to detect HIV in the HIV-positive group, after all other factors have been controlled for (eg health status).  No, this doesn't prove a universal negative, but if the control group is large enough and the study is conducted to high enough standards, such a result would be enough to strongly suggest that in all likelihood, HIV could not be found in anyone not at risk for HIV, particularly if the results were demonstrated to be reproducible.

A good place to start might be with the O'Hara study I cited earlier, which demonstrated the opposite:  Even in a small sample group, "HIV particles" were found in nearly 87% of patients with non-HIV lymphadenopathy, as well as in a similar percentage (90%) of patients with HIV lymphadenopathy.  (O'Hara CJ, Groopmen JE, Federman M. The Ultrastructural and Immunohistochemical Demonstration of Viral Particles in Lymph Nodes from Human Immunodeficiency Virus-Related Lymphadenopathy Syndromes. Hum Pathol 1988;19:545).  Science is for the most part more about questions than answers, and a good question to ask at this point is, "What separates the putatively 'viral' particles found in the lymph nodes of patients with HIV lymphadenopathy from the seemingly-identical particles found in patients with non-HIV lymphadenopathy?"  Or alternately, are they the exact same particles, be they retroviral or otherwise?

If the latter be the case, then that proves conclusively that the particles known as "HIV" are endogenous and are commonly found in the lymph nodes of most or all humans with lymphadenopathy, regardless of an individual's HIV status or AIDS risk, and for that matter, regardless of whether the particles are truly retroviral at all.

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

P.S.  Thanks for the reference to the name of Montagnier's patient in the sidebar, BTW.  Just having the name you gave me has re-opened a line of investigation that had ground to a halt more than a year ago.  It'll take me at least a week or so to respond to that sidebar, as I have to wait for the delivery of some books and other research materials and then digest it all, but I'm learning some surprising and fascinating stuff (and I think some stuff that'll suprise you too.)

--- G

Indeed, HIV depends on perinatal, instead of sexual, transmission
for survival—just like other animal and human retroviruses. Therefore,

the efficiency of perinatal transmission must be high.

On Duesberg:

That article I sent, as I said, partially makes Duesberg's argument that HIV is an ordinary endogenous retrovirus.  It does not contain the whole argument.  The one and only place I know where the entire argument can be found is in his book, Inventing the AIDS Virus, and I couldn't even give you a page number, since the whole of the argument is spread over the book.

And I do have to admit that I cannot find a reference to Duesberg directly making the specific claim that HIV is endogenous.  There is, of course, discussion of endogenous retroviruses in some of his papers, such as Retroviruses as Carcinogens and Pathogens: Expectations and Reality, but most of the papers at his site that even use the word "endogenous" were authored by other scientists with whom Duesberg holds strong disagreements on the existence issue.  So it's every bit possible that by using the word "endogenous", I'm putting words in his mouth.

However, his description of the nature of HIV is consistent with the Wiki entry on endogenous retroviruses, (which, so far as I can tell, is generally consistent with current accepted theories on ERVs,) in that he contends that HIV is a very old virus which is primarily transmitted perinatally, and which is generally not infectious in the conventional sense, and therefore not contagious, or at least not readily so.

On O'Hara:

Unfortunately, the first three years or so that I was researching these issues, I hadn't yet adopted the habit of saving copies of articles that I read.

Here's a link to the abstract.  If you want to read the full article and there's any cost associated with it, I'll absorb it in order to have a copy for myself.

According to the abstract, the one thing that in the researchers' minds set the "HIV" particles apart from the "non-HIV" particles is the apparent presence or absence of p24, which itself has proven to be non-specific to HIV, in that p24 can be found in the cells of healthy persons and animals uninfected by HIV.  Indeed, as I pointed out earlier, nearly half of all dogs have been demonstrated to test seropositive for p24 on the Western Blot, suggesting current or prior exposure to p24, despite the fact that it is highly unlikely that 43% of all dogs have or have ever been exposed to Human Immunodeficiency Virus.

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

But because only 1 in 100 T-cells are ever infected in humans, virtually all such studies use Kary Mullis' polymerase chain reaction, a technique that is designed to amplify a DNA-needle into a DNA-haystack. Such efforts have confirmed the existence of HIV-specific DNA in most (not all) antibody-positive persons with and without AIDS - but not in the DNA of antibody-negative people. For example Jackson et al have tested blood of 409 antibody-positives including 144 AIDS patients and 265 healthy people. In addition 131 antibody-negatives were tested. HIV-specific DNA subsets - defined in size and sequence by HIV-specific primers (start signals for the selective amplification) - were found in 403 of the 409 antibody-positives, but in none of the 131 antibody-negative people (16).

Jean-Marc,

This touches on a subject on which I am most critical of Duesberg.

Duesberg makes mention of the unreliability of HIV tests, and acknowledges that false-positives exist, but rarely if ever explores the possibility of false positives in any particular case or study.  Thus, it comes as little surprise that he assumes all of the antibody-positives in the Jackson study to have been true positives, despite the fact that this is statistically unlikely.

He makes a similar assumption in the case of Kimberly Bergalis.  Despite the fact that respiratory tract infections, flus, and viral infections can cause false-positives (Challakere K, Rapaport M. 1993. False-positive human immunodeficiency virus type 1 ELISA results in low-risk subjects. West. J. Med. 159(2):214-215), and that Bergalis was diagnosed while in the throes of pneumonia, he never raises the question of the validity of Bergalis' HIV test, and instead assumes that she actually had HIV, and that she possibly got it from her mother perinatally.  His "proof" for this thesis is most disappointing in this case:  Bergalis' mother was never tested for HIV, therefore she might have had it, therefore that must be where Bergalis got it.  (See Inventing the AIDS Virus pp 348-354.)

He does similar disservice to logic in the case of Ryan White.  Others have pointed out the likelihood that White was a false positive, but Duesberg never raises the question of White's true HIV status.  Instead, he asserts that if White had HIV, that he carried it harmlessly, and that he was instead killed by AZT, impure Factor VIII, and hemophilia.  (Inventing pp 287-288) 

This is why give Duesberg the bulk of the credit for convincing me that HIV probably doesn't exist.  If you actually read much of his work, you'll find that, generally, he makes a point to document his arguments very thoroughly.  Yet, where it comes to the existence issue (referring both to the larger existence issue and also to the issue of whether HIV is present in a given individual case, such as Bergalis or White,) his arguments are poorly-documented and fraught with needless assumption.  He assumes, for example, that Bergalis had HIV, despite the high probability that she was false positive instead.  Indeed, in his re-telling of the Bergalis story, he uses the word "unproven" to refer to HIV tests, and yet he still never once raises the question of the accuracy of Bergalis' diagnosis.  As a result, he documents thoroughly his argument that she couldn't have acquired HIV from her dentist, without ever considering whether she actually acquired HIV at all, whether from her dentist or, as Duesberg suggests, from her mother.

I've said it about orthodox scientists and I'll say it about Duesberg:  In science, when you assume anything, you make an ass out of u and me.

As to Duesberg's assertion that AIDS in the West is primarily caused by prolonged or excessive drug use, it is my feeling that he is the proverbial blind man describing the elephant as serpentine, based on what he can feel of its trunk.  Can drugs cause AIDS?  In my experience and research, I have become convinced that they can.  Are they THE cause of AIDS, as Duesberg seems to suggest?  Considering that no member of the Rolling Stones has died of AIDS, (not to mention many others who have used drugs heavily for decades without getting AIDS, many of whom have lived to a ripe old age despite drug abuse,) I am convinced that other co-factors must be involved in most cases.  In other words, in most cases drug abuse is neither necessary nor sufficient to cause AIDS in the absence of other co-factors.  I am, however, convinced that certain drugs, such as crystal meth, antibiotics, corticosteroids, ARVs, and nitrite inhalants, are sufficient to cause AIDS in the absence of co-factors (including the absence of HIV itself), particularly if taken in combination, but typically only with heavy, prolonged, and/or excessive use.

Is there a correlation between drug abuse and AIDS?  Among HIV-positives, it is generally accepted that there is.  In fact, in a "Living with HIV" course that I took shortly after testing positive, we were told that HIV-positives who abuse drugs tend to progress more quickly to AIDS, and that if we simply avoided drugs, we could reasonably expect to live 10 years or more after initial infection.  Drugs were thus presented as an AIDS "co-factor", extremely instrumental in the progression to AIDS after initial infection, in a strictly orthodox context.  Thus, I need not cite Duesberg at all in an assertion that drugs are an AIDS co-factor, since this has been the widely-accepted position of the orthodoxy for at least nine years that I personally know of.

Now, as to how I interpret such faults in a scientist's arguments, whether we're talking about Duesberg or Gallo or any other, when I see such things, I begin to look for a pattern, if it's a scientist whose writings I've studied rather extensively.  Where else can this pattern of thought be found in his arguments, and what are the implications to his larger argument, and to the arguments of his detractors?

In Duesberg's case, the pattern I've observed is that Duesberg indulges in assumption wherever he feels that such an assumption needs no defense, because it is widely accepted.  Thus, because it is widely accepted that Bergalis had HIV, he assumes she had HIV and quibbles only with where she might have gotten it, and this is one of many examples I could list of him making such assumptions.

However, in his more controversial stances, particularly on the issue of whether HIV is the cause of AIDS, he is meticulous in his documentation, and more compelling with his arguments, and this is due in no small part to the fact that he assumes nothing in such cases -- if he can't document it, he doesn't say it, and having personally tracked down more of Duesberg's citations than any other scientist I've ever investigated, I can attest that when he cites an article, you can find his assertion almost verbatim in the cited document.

Does his comment on Jackson surprise me?  Nah.  Do I think he's right?  No, I think it's just another case of Duesberg assuming what it's safe for him to assume -- in essence, practicing science by selective exegesis.  In true Duesberg form, he assumes that the Jackson study is valid on its face, and never considers the fact that at least some of the HIV-positives in the study (a statistical average of 98 out of 409, according to what we established earlier of the accuracy of the EIA/WB algorithm of the period,) should have been false-positive and therefore HIV-negative, thus calling into question how it would be possible to co-culture HIV from their cells to begin with.

I don't know about you, but as for me, I tend to be more critical of the opinions of scientists I strongly agree with, than of those that I strongly disagree with.  It is both a failing and a strength:  It is a failing in that I tend to be more dismissive (and therefore less likely truly critical) of the opinions of scientists that I hold strong disagreement with, but it is a strength in that I can be extremely critical of the opinions of those I strongly agree with on key points, and thus explore the pitfalls in their and my own arguments for or against a given hypothesis.

Because of this, I am probably more critical of Duesberg than you are, in all honesty, as many dissidents are.  If you want to get in a bitch session about Duesberg, I could talk your ear off, and I could certainly keep it up far longer than I could if the subject were Gallo instead, because I know more about his flaws as a scientist than I do about Gallo.

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

Jean-Marc,

I'm not quite sure what you're referring to, but what I think you might be referring to is the assumption that the 409 antibody-positives represent a portion of a random sampling of Americans.

And while you do have something close to a point (assuming, of course, that I'm guessing correctly about what you're referring to,) in that if the sampling were from a subset of Americans with a much higher seroprevalence than average, then there would be fewer false positives, that point is specious in that it assumes that we can predict seroprevalence based entirely on assumptions which in turn are based on prejudice rather than scientific evidence.

This tendency towards prejudice and assumption is a subject I intend to deal with when I return to the subject of Montagnier's patient, but first I have to wait for a book to arrive by mail and read it.  In the meantime, suffice to say that the "viral particles" which were supposedly found in Frederic Brugiere did not come from Brugiere at all; the Pasteur Institute acknowledged in 1991 that they were only present in his sample as a lab contaminant, and that they are believed to have come from another patient whose name was Cristophe Lailler.  (More on that later when I've actually read the book -- and actually, it's just become two books, because I just found another book that includes excerpts from Montagnier's own notes -- some of them in his own handwriting.)

As for your cricism of my math concerning the HIV epidemic in France, I challenge you to plot a course for the French HIV epidemic which:

a)  Shows a bell curve consistent with Farr's Law.

b)  Results in not much more than 69,000 cumulative infections by 2005 (I'll give you a little leeway with that number, since it cannot be assumed that there were no unknown cases.)

c)  Results in an average of 5,500 new infections per year in 2003-2005.

d)  Stretches the epidemic all the way back to the early 1980s, leaving enough cases in France at that time for there to have been any significant likelihood that either Brugiere or Lailler actually had HIV.

Quite frankly, I know that my math on the French epidemic was wrong -- it was the only way I could fulfill items b and d.  There simply aren't enough cumulative cases to stretch the epidemic back that far and still leave more than a handful of people (indeed, even one) who could possibly have been infected in the whole country of France in the early '80s.  However, you are more than welcome to try to come up with a better estimate yourself.  I submit that you cannot do it, because it cannot be done.  You'd have to double the cumulative total just to stretch the epidemic back beyond 1990, and it's still doubtful that you'd have enough room to include a Farr bell curve, unless you assume that HIV has not yet hit its peak in France, in which case the curve would be so long and slow that it would show only a handful of cases in France for the entire decade of the 1980s.

--- Gos

--- gos@nerosopeningact.com

"Nobody here but us heretics..."

I'm stumped -- what is it?

Here are the books:

History of AIDS:  Emergence and Origin of a Modern Pandemic by Russell C. Maulitz

Science Fictions:  A Scientific Mystery, A Massive Cover-up, and the Dark Legacy of Robert Gallo by John Crewsdon

http://www.amazon.com/Science-Fictions-Scientific-Mystery-Cover-up/dp/0316090042/ref=sr_1_1?ie=UTF8&s=books&qid=1200121915&sr=8-1

I've already ordered the second one -- I'll order the first next payday.

--- Gos

Kewl.

So -- am I gonna die of curiosity so that the coroner can blame HIV for my death, or are you gonna answer my questions?  :)

1)  What is the assumption that you're referring to in my analysis of the Jackson paper?

2)  Can you spread 69,000 cumulative infections over a 25-year period and come up with something better than lottery odds that any given gay man with lymphadenopathy in a country with 56 million people actually has HIV?

--- Gos

Gos,
"So -- am I gonna die of curiosity so that the coroner can blame HIV for my death, or are you gonna answer my questions?  :)"
Ha! :-)  It is 5:45am here and I almost woke my up from snorting too loudly at that.  Sorry about the delay.  Like I said I have been really busy.
Here we go.

1) Assumptions

• The 409 people are representative of the entire population as a whole (You mentioned this assumption and it is a major one I did not initially take into account but there is another)
• All 409 patients have an equal chance of being false positives (this is one you don't mention)

What we actually have is not a random sampling of a low risk population nor is this evidence that seropositivity alone can give us 409/409 correct results in an experiment such as this.
Remember of the 409 individuals, 144 were already symptomatic with either AIDS or ARC.  These by definition would be expected to be HIV positive so it is no surprise that their results show this.  Now we are left with a set of 265 individuals from high risk groups who went to get tested for HIV and not only tested positive on ELISA but also on WB.  So these are not 409 random samples at all and this throws off your math in a major way.  Thus, your extrapolation of unknowns from high risk groups from those of a low risk population (even by your own admission) and use of wrong sample size would make your mathematical approach to refuting this very much incorrect.   So now, bearing in mind that the  144 symptomatic patients are  expected to be positive you must calculate the odds of the remaining 265 being double false-negatives (ELISA and WB).  This takes us back to the specificities we had used previously; 98.5% ELISA and 91.6% WB.
Thus of our 265 possible false positives, we could expect that 0.126% of them or ~0.3) would have been falsely identified negatives.


2) Are you referring to the Montagnier paper here?

As for Farr's law I have a question for you:
What assumptions are made of an infectious organism's characteristics in order for it to propagate according to Farr's law?

-JM