Correcting Gallo: Rethinking AIDS Responds to Harper’s ‘Out of Control’ Critics

Version 1.4.1: September 27, 2006.

In its March, 2006 issue, Harper’s magazine published “Out of control: AIDS and the corruption of medical science”, an article by Celia Farber which described the death of one woman in a US-based clinical trial of Nevirapine in pregnant HIV-positive women, and the shoddy, corrupt or perhaps outright fraudulent trial of the same drug in Uganda. She described the coverup that occurred, and raised important questions about the effectiveness and safety of HIV/AIDS research. For brevity we will refer to this as “the Farber article”.
Shortly after this article was published, on March 3rd to be exact, a document started circulating entitled “Errors in Celia Farber's March 2006 article in Harper's Magazine”. Half of its authors were researchers: The lead author was Robert Gallo, MD, who claims to have discovered HIV. Others were microbiologist John Moore PhD, of Cornell University , Jeffrey Safrit PhD, senior program officer for the Elizabeth Glaser Pediatric AIDS Foundation (which receives money from the Nevirapine manufacturer) and a medical professor, Daniel Kuritzkes MD. The remaining four are activists for AIDS drug treatment, HIV vaccines and medical marijuana. We will refer to this as “the Gallo document”.
After the Rethinking AIDS response the website “AIDSTruth.org” wrote that they “are aware that the AIDS denialist group, Rethinking AIDS, has finally prepared what they deem to be a rebuttal of our exposure of the errors perpetrated by Celia Farber in her Harper’s Magazine article. We have looked over the AIDS denialists’ response. It is characteristically superficial and silly, further exposing the Rethinking AIDS group’s misunderstanding of the science of HIV/AIDS. We will not be responding further to it. The AIDStruth website will continue to post, at periodic intervals, information that is relevant to understanding how HIV infection causes AIDS and how AIDS can be treated with anti-retroviral drugs.”
We would be happy to enter into a constructive debate but this response to our detailed scientific survey indicates that they are unwilling or, more likely, unable to respond to our challenges with substantive science of their own.
The Gallo document claims to have noted 56 errors in the Farber article. The purpose of this website is to address all of these. For each supposed error, relevant text from the Farber article is given, followed by the error description from the Gallo et al document, and then our response, including references identified as “RA”.

Our analysis of the Gallo et al document attacking the Celia Farber article in the March, 2006 issue of Harpers magazine is broken down into the following sections. In each file a quotation from the Farber article is marked as “Farber”, the entire text of the Gallo document is marked as “Gallo” and our response is marked as “RA” (Rethinking AIDS). When we supply a section of references they are marked “Refs.”:

The Gallo Document(s)

We have discovered four versions of the Gallo document on the internet, dated March 3^rd, March 4^th, March 22^nd and March 25^th. The last two are marked “Final”. We have not analyzed the differences, however the two ‘final’ versions included the following note:

Correction History [for Gallo et al] 3 March 2006: First public version. Sent to Harper's. 4 March 2006: Modified (37;3) "Nevirapine remains an important antiretroviral medicine whose risks outweigh its benefits." to "Nevirapine remains an important antiretroviral medicine whose benefits outweigh its risks." (b) Modified Bruce Mirken affiliation. 5-25 March: references standardised and typing errors corrected. Thank you to Sister Mary Elizabeth of AEGiS for assisting with these changes. This version is final.

We have not modified the four files linked above except the first file includes the number of each of their comment.

Rethinking AIDS Responds to the 56 ‘Errors’

Introduction to the Gallo Document

Item #1: Pregnancy and False Positive HIV Tests

Item #2: “Outer limits of bearable toxicity”

Item #3: Is the Death of One Person Relevant?

Item #4: HIV Antibodies in Babies

Item #5: Problems with HIV Tests

Item #6: Comparing Clinical Trial PACTG 1022 to HIVNET 012

Item #7: Are reports of PACTG 1022 Sinister?

Item #8: Comparing Clinical Trial PACTG 1022 to HIVNET 012

Item #9: Is it Okay That the Elizabeth Glaser Pediatric AIDS Foundation Takes Money from the Nevirapine Manufacturer?

Item #10: The Definition of AIDS in Africa

Item #11: Does HIV, not Poverty, Predict Progression to AIDS in Africa?

Item #12: Are HIV Tests Widely Used in Africa?

Item #13: Tropical Diseases and False Positive HIV Tests

Item #14: African HIV/AIDS Statistics

Item #15: Who Benefits from Clinical Trials?

Item #16: Is Jonathan Fishbein Qualified to Comment on HIVNET 012?

Item #17: Nevirapine Rejected by Canada…Twice

Item #18: Did HIVNET 006 Lower Viral Load?

Item #19: 4 of 22 Infants Died in HIVNET 006. Is this a Problem?

Item #20: HIVNET 012 Protocol Changes

Item #21: HIVNET 012: Phase II or Phase III?

Item #22: HIVNET 012 Not Placebo Controlled

Item #23: Hopkins Medical News Hyping Nevirapine?

Item #24: Farber’s Description of HIVNET 012

Item #25: HIVNET 012 Participants Also in a Vitamin A Trial

Item #26: Was the IOM Report Biased?

Item #27: IOM Report Writers Received NIH Grant Funding

Item #28: Maternal Nevirapine Proven in ‘Multiple Studies’?

Item #29: Valendar Turner, Nevirapine and Placebo

Item #30: Nevirapine and a Study with 561 People

Item #31: Vitamin A and HIV Transmission Rates

Item #32: BW 002 Study of AZT

Item #33: Problems with Original AZT Studies

Item #34: Why was BW 002 Aborted?

Item #35: Was ddI Approved without a Clinical Trial?

Item #36: Was Indinavir Approved Without a Clinical Trial?

Item #37: Are Clinical Trials Improving with Time?

Item #38: How Does AZT Work?

Item #39: Does HIV Cause Disease by Killing CD4 Immune Cells?

Item #40: Does HIV Fulfil Koch’s Postulates for AIDS?

Item #41: 4,000 AIDS Cases without HIV?

Item #42: Is HIV Active in the Bodies of AIDS Patients?

Item #43: Can HIV be Isolated Without ‘Reactivating’ Latent Copies?

Item #44: Antibodies Mean Immunity…Except for HIV?

Item #45: Does ‘Viral Load’ Measure Live Virus?

Item #46: The HIV Latency Period (Time Before AIDS Develops)

Item #47: Does HIV Spread Randomly? Should it?

Item #48: Remote Cell ‘Suicide’ (Apoptosis)

Item #49: Genetic Immunity to HIV

Item #50: Does HIV Kill T-Cells?

Item #51: HIV Does Not Kill Chimpanzees

Item #52: Non-HIV Causes for AIDS

Item #53: HIV and Holocaust ‘Denialism’

Item #54: Scurvy as a Parallel to HIV/AIDS?

Item #55: The Reappraiser’s Petition

Item #56: Does AIDS Drug Toxicity Cause AIDS?

 

Introduction to the Gallo Document

Gallo	Our primary concern is with rebutting Farber’s misconceptions about HIV/AIDS and antiretrovirals (ARVs). We have not focused our attention on misleading or biased reporting that relate to the NIH; none of us is an NIH employee. We have also ignored the sections on Peter Duesberg’s career problems, his rejected funding proposals, and how he is (or is not) regarded by other cancer researchers nowadays; we have no interest in Duesberg, other than to note that he is not an AIDS researcher and has no practical experience in studying HIV. Using a plethora of false, misleading, biased and unfair statements, Farber attempts to cast scientific institutions and scientists as dishonest. But intellectual dishonesty is the norm for Farber and other AIDS denialists including David Rasnick, Peter Duesberg, Kary Mullis and Harvey Bialy – all people she mentions favourably in her article. David Rasnick works for a vitamin entrepeneur, Matthias Rath. They have conducted unauthorised experiments on people with HIV in South Africa, convincing their subjects to take Rath‘s vitamin products in dangerously high doses, instead of scientifically recognised treatments for AIDS. It has been alleged that some of their subjects have died due to this experiment 1 . Farber implies financial motives permeate scientific research. Why does Farber not make similar allegations against the AIDS denialists, many of whom are involved in the marketing of unproven alternative medicines? HIV has been shown to be the cause of AIDS in numerous studies. ARVs have been shown to reduce death and illness in people with HIV. They have also been shown to reduce mother-to-child transmission (MTCT) of HIV. They often cause side-effects. On rare occasions these can be fatal, but death from HIV/AIDS is a far greater risk. The evidence shows beyond doubt that the benefits of ARVs far outweigh their risks.
RA	While not included as one of the 56 ‘errors’, the Gallo attempts to impugn the character, qualifications and credentials of the AIDS ‘dissidents’, ‘denialists’ or, as we would prefer, ‘rethinkers’ interviewed by Celia Farber: Dr. Peter Duesberg, Dr. Kary Mullis, Dr. David Rasnick and Dr. Harvey Bialy. The first sign of bias is the omission of their scientific credentials, including the prefix “Dr.” or suffix “PhD” – “David Rasnick” rather than “Dr. David Rasnick” or more specifically “David Rasnick, PhD”. By contrast, they purposefully mention that Robert Gallo and Daniel Kuritzkes are MDs and that John Moore and Jeffrey Safrit have PhDs. David Rasnick is described as performing unethical experiments for a “vitamin entrep[r]eneur”. They neglect to mention that he is a PhD research scientist with a background in protease inhibitor drug development. Yes, an expert in the very drugs that, in the mid-1990s, were going to revolutionize the treatment of AIDS. Sadly, after a brief period of hype, serious side effects started to emerge, fatal in too many cases. Rasnick no longer believes that the drugs he is an expert on have a place in treating AIDS. The authors mention Duesberg’s funding troubles, insinuating that this is a dismal reflection on his qualities as a scientist. However, within modern scientific institutions, funding and publication is decided by anonymous peer review. It is common and profitable for the majority (with lab, salaries and ability to publish dependent on HIV/AIDS) to exclude a minority of troublesome scientists who refuse to go along with their dogma. Duesberg was shut down after publishing a major paper in 1987 claiming that HIV does not cause AIDS. The Gallo document claims that Duesberg is “not an AIDS researcher”. This is an incredible statement. Robert Gallo has previously stated that Duesberg is one of the world’s leading retrovirologists. He has won many prestigious grants and awards. Apart from three books on HIV/AIDS, a PubMed query on “Duesberg P[au] AND (HIV OR AIDS)” reveals 34 scientific publications. A similar search for papers on retroviruses reveals 151. A search on papers related to cancer or tumors reveals 113, dating back to 1966. At the back of the Gallo document, just before the references, the authors do admit that Kary Mullis is a nobel laureate. What they don‘t tell you is that he won the 1993 Nobel for Chemistry – for the invention of the Polymerase Chain Reaction nor do they reveal that he opposes the use of the manufacturing technique as a test for HIV. Mullis admittedly has some other unusual views which he is very open about. It would be a terrible day for science if everyone with unorthodox ideas was excluded from scientific discussions. Were that the case, Einstein’s crazy ideas, e.g., how time slows down if you travel real fast, would have excluded him from the inner circle of scientists, not catapulted him into it. At the back of the Gallo document is the information that Harvey Bialy was the founding scientific editor of the journal Nature/Biotechnology. They state “He no longer holds any position with Nature” which seems to imply that he did something wrong, when he simply retired and moved onto other positions. The authors fail to mention that Robert Gallo no longer holds any position with the National Institutes of Health, a much more interesting story, which will get to in a momemt. This character assassination would be more successful if all the authors of the Gallo document were scientists. Half of them, however, are AIDS drug treatment advocates. Pubmed queries on Nathan Geffen reveal 0 (zero) scientific papers on any topic. Gregg Gonsalves has 21 Pubmed-indexed news articles listed (omitting three scientific papers on turtles, presumably by a different G. Gonsalves), mostly in the Gay Men’s Health Crisis newsletter. Richard Jefferys had 11 hits on HIV or AIDS, all news articles, all but three in the Body Positive newsletter. Bruce Mirken has 31 news articles and letters listed in PubMed and one document that might be a scientific paper. All but three of these documents are in two AIDS treatment newsletters (AIDS Treatment News and BETA, the Bulletin of Experimental Treatment for AIDS). The other half of the authors – Kuritzkes, Safrit, Moore and especially Gallo – do have many scientific publications to their name. Robert Gallo has a different problem, the quality and validity of his scientific output. Probably no scientist in recent memory has been the subject of more investigations. An entire book was written by John Crewdson, Chicago Tribune science journalist, called “Science Fictions: A Scientific Mystery, A Massive Cover-Up, and the Dark Legacy of Robert Gallo” [1]. A chapter on the Gallo affair from Yale Mathematician Serge Lang’s book Challenges can be found at duesberg.com/viewpoints/gallocase-content.html. A Staff Report to the US House of Representatives Subcommittee on Oversight and Investigations is at www.healtoronto.com/galloindex.html. A scientific report on errors and false claims in retrovirology, mostly in Gallo’ lab, by virologist Abraham Karpas, has recently been published [2]. While the numerous investigations into Gallo’s research are impossible to describe briefly, a good summary is in the New York Times review of Crewdson’s book: “Science Fictions is bursting with allegations leveled at Dr. Gallo, his associates, rivals and enemies, that include deception, misconduct, incompetence, fraud, sabotage, back-stabbing, double-dealing, overstatements, half-truths, outright lies, a clandestine affair with a co-worker, a bribery attempt, denials, evasions, coverups and serial rewritings of history”. We are not averse to non-scientists investigating HIV and AIDS, in fact we encourage it. We are, however, concerned that the eight Gallo document authors should attempt to belittle the accomplishments of Farber’s sources – Rasnick, Duesberg, Mullis and Bialy. All four hold PhDs. All are well-published, legitimate scientists. All have a right – indeed, an ethical obligation – to comment on HIV and AIDS.
Refs.	Crewdson J. Science fictions: A scientific mystery, a massive cover-up, and the dark legacy of Robert Gallo. Little, Brown. 2002. Web: sciencefictions.net Karpas A. Human retroviruses in leukaemia and AIDS: reflections on their discovery, biology and epidemiology. Biol Rev Camb Philos Soc. 2004 Nov; 79(4): 911-33.

 

Item #1: Pregnancy and False Positive HIV Tests

Farber	[Hafford] did not know that pregnancy itself can cause a false positive HIV test
Gallo	Farber states that pregnancy itself can cause a false positive result. She supplies no supporting reference. A properly conducted HIV-test protocol (which involves at least two HIV tests) has a very small chance of giving a false positive, irrespective of pregnancy status. Farber alleges that Hafford's HIV-test was carried out incorrectly. If this was the case, medical negligence is a different matter to whether HIV tests carried out according to protocol are accurate in pregnant women. HIV tests were highly accurate from the time they were developed in 19842 and have become much more accurate over time as the underlying technology has evolved. HIV tests are amongst the most accurate available in medical science. For more on testing see Mirken (2001)3. For a more technical discussion see Coon (2000)4 . Incidentally, the testing protocol of the PACTG 1022 trial, to which Farber refers, required multiple HIV tests and regular viral load counts. Farber states that Hafford was only tested once. Assuming Farber is right, then Hafford's doctor did not follow the protocol. We, however, are not privy to Hafford's medical records and therefore cannot know if Farber's allegation of Hafford having only one test is correct. Was Harper's privy to this? Consequently, was the allegation fact-checked?
RA	The risk of a false positive HIV test is well documented in the scientific literature: “False-positive ELISA [antibody] test results can be caused by alloantibodies resulting from transfusions, transplantation, or pregnancy, autoimmune disorders, malignancies, alcoholic liver disease, or for reasons that are unclear...As the number of women being screened has increased, the proportion of false-positive and ambiguous (indeterminate) test results has increased and the positive predictive value (PPV) [a mathematical expression of the probability that a positive test is a true positive] of the standard HIV test has decreased” [1] “potential causes of indeterminate Western blots for HIV-1...included...HLA antibody cross-reactivity, and current pregnancy...All but one of the cases who demonstrated anti-class I HLA reactivity were multiparous women [pregnant more than once]” [2] A report in an American Medical Association newsletter: “New York health officials are facing an unexpected hurdle in their efforts to identify newborns whose mothers may have exposed them to HIV in utero. A state regulation went into effect in August 1999 that requires hospitals and birthing centers to test within 48 hours all women who present for labor and whose HIV status is unknown. Under the new requirements, babies are routinely screened at birth with the same test if their mothers decline it. But such tests are not always accurate and used appropriately. Preliminary health department data for August through November 1999 showed that screening with a rapid HIV test identified 32 HIV-positive women. After using a confirmatory test, however, 17 women were later determined to be HIV-negative. In the meantime, 13 of the 17 babies were started on preventive antiretroviral treatment. Babies treated with zidovudine, the standard preventive therapy, can develop anemia. The long-term effects of the drug are unknown…A pilot study conducted for research purposes last summer [1999] at a Bronx hospital found an "unacceptably high number" of false-positives, said Montefiore Medical Center epidemiologist Mayris P. Webber, DrPH, who was involved in the study. "One should be cautious in interpreting the results of a small pilot study of 100 women," she said, "but we did find, nonetheless, that out of three positive tests, two were false-positives." The predictive value of the test in a low prevalence population can be poor, she said…A study by the New York City Dept. of Health found a 45% false-positive rate for SUDS, said Sara T. Beatrice, PhD, the department's director of retrovirology and immunobiology” [3] A test kit manufacturer writes: “nonspecific reactions may occasionally be seen in specimens from people who have prior pregnancy, blood transfusion, or exposure to human cells or media containing cultured HIV antigen…when the ELISA is used to screen populations with a low prevalence of HIV infections, nonspecific reactions may be more common than specific reactions” [4] “The medical records of all rapid HIV-ELISA-positive gravidas [pregnant women] that delivered at our hospital between January 2000 and October 2001 were retrieved...The results of the Western blot tests were also retrieved and correlated to the ELISA results, across varying maternal characteristics....A total of 69 patients had a positive rapid HIV-ELISA out of 9,781 deliveries. Of those, 26 were confirmed as HIV infected by Western blot (overall HIV prevalence: 0.27%, ELISA-positive predictive value: 37.7%). The subgroup prevalence of HIV and positive predictive value of ELISA were 1.53 and 75% among Caucasians; 2.43 and 82.6% among African-Americans; and 0.05 and 9.8% among Hispanics, respectively…The positive predictive value of rapid HIV-ELISA during pregnancy varies widely, depending on maternal race/ethnicity and sexual behavior. The routine disclosure of rapid intrapartum HIV serum screening results prior to Western blot confirmation should be avoided in very low-risk populations. [and since there is generally no further confirmation of a positive Western Blot, it is actually impossible to tell whether these are true positives or not]” [5] “False-positive HIV ELISAs occur because of human or technical errors associated with doing the tests or because of antibodies that coincidentally cross-react with HIV or nonviral components in the tests…Notable causes of false-positive reactions have been anti-HLA-DR antibodies that sometimes occur in multiparous women and in multiply transfused patients.” [6] “Most patients (68 to 89%) from low risk groups (prevalence of 0.1% or less) who show reactivity on screening tests will have false-positive results…The predictive value of a positive ELISA varies from 2% to 99%…One notable association with false positive ELISA reactivity in some commercial preparations has been patients with anti-HLA-DR4 antibodies, most often multiparous [having experienced one or more births] or multiply transfused patients...the Western blot method [used to confirm these false positive ELISA tests] lacks standardization, is cumbersome, and is subjective in interpretation of banding patterns.” [7] “We selected the 20 most strongly [indeterminate or atypical Western Blot] reactive samples for further evaluation…Atypical WB [Western Blot] patterns in 19 of 20 of our donors remained substantially the same over time…our data show that the presence of p24 alone in WB should not be regarded as a false positive without subsequent testing of the individual…All study donors had normal immune status…[2] donors were multiparous females [multiple children], and one other probably had received a blood transfusion…we observed a large proportion of individuals who had either lived or worked on dairy farms (6/16) and frequently drank unpasteurized cows’ milk (7/16)…undefined autoimmune phenomena [such as multiple pregnancies], bovine exposure, or cross-reactivity with other human retroviruses could be possible causes for consistently reactive HIV immunologic assays” [8]
Refs	Doran TI et al. False-Positive and Indeterminate Human Immunodeficiency Virus Test Results in Pregnant Women. Arch Fam Med. 2000 Sep/Oct; 9: 924-9. Celum CL et al. Risk factors for repeatedly reactive HIV-1 EIA and indeterminate Western blots: a population-based case control study. Arch Intern Med. 1994 May 23; 154: 1129-37. Shelton DL. New York state physicians slam rapid perinatal HIV test. amednews.com. 2000 Mar 13. ama-assn.org/amednews/2000/03/13/hlsa0313.htm. Vironostika HIV-1 plus O microelisa system. Biomérieux. 2003 Jun 5. Zacharias NM et al. High false-positive rate of HIV rapid serum screening in a predominantly hispanic prenatal population. J Perinatol. 2004 Aug 19. Proffitt MR et al. Laboratory diagnosis of human immunodeficiency virus infection. Inf Dis Clin North Am. 1993; 7: 203-19. Steckelberg JM et al. Serologic testing for human immunodeficiency virus antibodies. Mayo Clin Proc. 1988; 63: 373-9. Dock NL et al. Evaluation of atypical human immunodeficiency immunoblot reactivity in blood donors. Transfusion. 1988; 28: 412.

 

Item #2: “Outer limits of bearable toxicity”

Farber	The objective of the trial, PACTG 1022, was to compare the “treatment-limiting toxicities” of two anti-HIV drug regimens…PACTG 1022 was a “safety” trial as well as an efficacy trial, which means that pregnant women were being used as research subjects to investigate “safety” and yet the trial was probing the outer limits of bearable toxicity.
Gallo	Farber states that PACTG 1022 probed the “outer limits of bearable toxicity”. PACTG 1022 compared ARVs, that had already been found to be safe and effective for treatment in the absence of pregnancy, in pregnant women. All drugs used in the trial had been shown in previous trials to benefit people with HIV. This is why the FDA has registered them. The PACTG 1022 trial happened to find higher than expected toxicity of nevirapine in very specific circumstances. Even here, toxicity was sufficiently rare as to be outweighed by the likely benefits of nevirapine use. The FDA revised its nevirapine recommendations on the basis of this trial. Nevirapine remains an important antiretroviral medicine whose risks outweigh its benefits. Nevirapine (or a drug, efavirenz, used instead of it) has been shown in an analysis of clinical trials to slow disease progression, particularly in patients with low CD4 counts. 5 Safety trials are obviously associated with a calculated risk, but they are permitted when the expected benefits are considered to outweigh this risk. Would Farber suggest that no clinical trials be conducted whatsoever?
RA	We know that the text in blue is a typographical error in the Gallo document, which was corrected in a later version, but we definitely agree with the latter part of the statement.
RA	This is patently false, and egregiously distortive. The FDA and equivalent regulatory agencies all across the industrialized world, in the late 1990s, rejected approval of nevirapine for the treatment of pregnant HIV positive women because of early reports of toxicities, maternal, and fetal deaths, including in pilot studies in South Africa. The FDA instructed Boehringer Ingelheim to withdraw its application to have NVP approved for maternal use after it reviewed the catastrophic HIVNET 012 study. To date, NVP is not approved by any industrialized nation for use in pregnancy. Canadian authorities rejected NVP not once but twice—in 1996 and again in 1998, finding it had no effect on surrogate markers and was “alarmingly toxic.” If Farber is incorrect and the study did not probe the “outer limits of bearable toxicity,” then why did the NIH specifically cite the study as one that tested the “treatment limiting toxicities,” of HIV drugs in pregnant women? [1] [2] In addition to the toxicities, deaths, and numerous warnings about NVP and “life threatening liver toxicity” in Farber’s Harpers article, beginning as early as 2000, additional data has emerged. These include but are not limited to one case of “Fatal Liver Failure with NVP” in a pregnant woman, whose baby’s fate was not cited. [3] In the “discussion” section of a paper in JAIDS titled “Maternal Toxicity With Continuous Nevirapine in Pregnancy: Results From PACTG 1022,” a total of six maternal deaths are cited from NVP use in pregnancy, with the first case reported in 2000. [4]
Refs.	Maternal Toxicity with Continuous Nevirapine in Pregnancy: Final Results From PACTG 1022 hivandhepatitis.com/recent/women/061804_c.html. http://clinicaltrials.gov/ct/show/NCT00017719?order=1. Note that the phrase “treatment limiting toxicities” was removed from this page some time in April or May, 2006. Langlet P, Guillaume MP, Devriendt J, et al. Fatal liver failure associated with Nevirapine in a pregnant HIV patient: the first reported case. Gastroenterology. 2000; 118: A1461. Hitti J et al. Maternal toxicity with continuous nevirapine in pregnancy: results from PACTG 1022. JAIDS. 2004 Jul 1. 36(3): 772-6.

 

Item #3: Is the Death of One Person Relevant?

Farber	Joyce Ann Hafford was thirty-three years old and had always been healthy…Hafford was on the drug regimen for thirty-eight days…[on] July 25, Hafford was summoned back to the hospital after her lab reports from nine days earlier were finally reviewed. She was admitted to the hospital's ICU with “acute and subacute necrosis of the liver, secondary to drug toxicity, acute renal failure, anemia, septicemia, premature separation of the placenta,” and threatened “premature labor.” She was finally taken off the drugs but was already losing consciousness.Hafford's baby, Sterling, was delivered by C-section on July 29, and she remained conscious long enough not to hold him but at least to see him and learn that she'd had a boy…In the early morning hours of August 1, Rubbie and her mother got a call to come to the hospital, because doctors had lost Hafford's pulse. Jermal was sleeping, and Rubbie woke her own daughter and instructed her not to tell Jermal anything yet. They went to the hospital, and had been there about ten minutes when Joyce Ann died.
Gallo	Farber describes the death of one patient and implies this is relevant to the science of HIV. To try to get readers to conclude that an ARV related death can be generalised to conclude that the risks of ARVs outweigh their benefits is misleading and unscientific. HIV is a life-threatening condition. The drugs used to treat it are imperfect but have been shown beyond reasonable doubt in numerous clinical trials and analyses of large numbers of patients in real-world settings (operational cohorts) to reduce the risk of illness and death. They are associated with side-effects. The same scenario applies to chemotherapy for cancer; patients take drugs that cause nausea, vomiting, hair-loss etc, because to do so is preferable to dying from cancer. Clinical trials, or meta-analyses of clinical trials, have demonstrated direct clinical benefits, i.e. fewer AIDS-related illnesses or deaths, for a number of ARVs, including AZT6, lamivudine7, didanosine8 , stavudine9, nevirapine10 , efavirenz11 and others. As ARVs began prolonging the lives and reducing the illnesses of people with HIV, it became the standard of care. In recent clinical trials the control group has to be given this standard of care for ethical reasons. Consequently progression to AIDS or death is unusual in recent clinical trials. Therefore scientists use what are called surrogate markers, CD4 and viral load counts, to determine drug efficacy. These surrogate markers are highly correlated with disease progression. 12 A meta-analysis of ARV trials has demonstrated that they have a profound effect on reducing progression to AIDS or death. 13 Furthermore, in practice, ARVs have been shown to reduce illness and deaths in industrialised and developing countries around the world irrespective of race, gender, sexual orientation, age and recreational drug use. We have included a sample of these in the endnotes. 14,15,16,17,18,19,20,21,22,23
Farber	First of all, Joyce Ann Hafford was not a “patient”, she was a healthy pregnant woman who once tested positive on an HIV test, before she was unceremoniously killed.  I didn’t “imply” anything by describing her death–I described her death, as it happened. I wasn’t “trying’ to “get readers to conclude” anything on the tortured scoreboard of ARV treatment choices that TAC et al believe is the only possible reason for reportage. I am not a treatment advocate. I don't work for TAC, and I don't work for the AIDS industry. I told the story because it happened. I felt the story said something about the current state of HIV culture, which has seemingly lost sight of the goal not to kill the patient. To date, no remorse has been expressed to Hafford's family from any of those responsible for her death, and no compensation has been offered. The only additional shock the family could possibly receive is to now learn that international AIDS "treatment activists" have declared Joyce Ann's death not "relevant to the science of HIV." That statement is sociopathic–bereft of all empathy. This is what I have long suspected AIDS treatment activists to be and this is what they say, in their own words, when given a chance to say something about this tragic death. Here, by contrast, is what Joyce Ann's sister, Rubbie King, said, in a letter to Harpers: "I miss her every day. I have not visited her grave or put flowers on it since we laid her to rest on August 6, 2003. The pain is so deep. Almost three years later, just thinking of her brings tears to my eyes. She was an incredible person, not a lab rat."
RA	The death of a single person in a clinical trial should be cause for concern, not for a cover-up. The death of Joyce Ann Hafford is not more or less important than the deaths of women and babies in the Uganda trials of the same drug but due to the poor management of that trial, and because these women are in a poor country far away, they remain anonymous. If known, their tragedies would be just as sad as the death of Hafford. AIDS researchers and treatment activists who do not consider a single death to be important should consider why they got involved in the first place. Their important claim that “A meta-analysis of ARV trials has demonstrated that they have a profound effect on reducing progression to AIDS or death” is backed up by a reference to a recent meta-analysis (analysis of the combined data from several studies) by Jordan et al [1]. The authors mentioned that “Zidovudine [AZT] was the only monotherapy [actually the only therapy of any kind] compared with placebo or no treatment.” Furthermore, the bulk of the data in that trial comes from the Concorde trial that concluded that AZT was not effective (it also wasn’t a true placebo controlled trial, Jorden et al admitted that “We classified immediate versus deferred zidovudine as zidovudine versus placebo.” However, this data source was too large to ignore (see Figure 2 in Jordan et al), and when combined with several smaller trials that generally showed much more positive results for AZT, a small, statistically significant benefit for AZT for placebo was teased out. So Jordan et al boils down to one study, the Concorde study [2] which states ”The results of Concorde do not encourage the early use of zidovudine [AZT] in symptom-free HIV-infected adults.”, hardly a ringing endorsement. Furthermore, Concorde merely compared AZT right away in one arm of the trial versus AZT after AIDS developed in the other arm. Drugs since AZT have not been compared against placebo, but against AZT or other older AIDS drugs, singly or in combinations. And in the Jordan et al paper, all other drugs were tested in this fashion, and so the meta-analysis just showed that drugs were killing fewer AIDS patients over time, a combination of A) lower dosages, B) drugs of less toxicity and C) people being diagnosed with milder disease or, since 1993, no disease at all. The best that can be said is that AZT has been shown, by trials of questionable methodology and validity, to have a small, short term benefit. As Jordan et al stated “as the trials increased in length zidovudine [AZT] had a smaller relative effect. At 152 weeks (about three years), as in the Concorde trial, the beneficial effect of zidovudine was virtually eliminated.”
Refs.	Jordan R et al. Systematic review and meta-analysis of evidence for increasing numbers of drugs in antiretroviral combination therapy. BMJ. 2002 Mar 30; 324(7340): 757. Concorde Coordinating Committee. Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Lancet. 1994 Apr 9; 343(8902): 871-81.
RK	To Whom It May Concern: My name is Rubbie N. King. I am the sister of Joyce Ann Hafford, now deceased. I am forever grateful to Harper’s Magazine and the writer, Celia Farber for the article in the March, 2006 story, “Out of Control, AIDS and the Corruption of Medical Science.” In early April, my sister was diagnosed HIV positive. She learned of this diagnosis in the early stages of her pregnancy. The opportunity to minimize or stop the transmission of the disease to her unborn baby was presented by her physician. She agreed to engage in the clinical trial study, PACTG 1022. Her therapy included Viramune (Nevirapine) and Combivir. From the early onset, I was concerned about the medications because there were no warnings with the Viramune. In addition to the unaccounted for warnings, when she began taking the drug, she experienced an allergic reaction almost immediately. She phoned her doctor. It was never suggested to her to stop taking the medicine. The idiots took her off the drugs when she was in life threatening danger. Unfortunately for her, it was too late. My sister delivered a 4 lb. 8 oz. baby boy. One she named while she carried him in the womb. She was the mother of an older son, who was then 13 years of age. She died three days later from the poison prescribed to her from the professionals who know medicine best. She never held her son. Her oldest son lost his best friend and the only mother he would ever have. A group of scientist and doctors who hide behind the shield of the NIH, government immunity and the other radicals that decide that they have more power than God were responsible for the underreporting of the deaths related to the Uganda study. This underreporting was the means by which the federal government would pour more funds into the study of AIDS. What I later learned, Boehringer Ingelheim and a few of the other doctors, employees of the NIH, made deals to hide the truth about the toxicities of Nevirapine and AZT. They received millions of dollars to lie (withhold information) to the FDA and the American public. My sister’s life meant nothing. In fact, my sister was just another single black guinea pig, whose life was deduced to nothing more than a “oops, not much we can do about dumb docs,” a quote from Ed Tramont, Director of the NIH. While this hit home for my family, I am left raising her two children, because what happened to her was no more than a “simple mistake” according to Tramont. It is the attitudes of the people like Robert Gallo MD, Nathan Geffen, Gregg Gonsalves, Richard Jefferys, Daniel R. Kuritzkes MD, Bruce Mirken, John P. Moore PhD, Jeffrey T. Safrit PhD and others like these people who misconstrue fact with fiction in that your goal is to minimize the importance of life and the quality of it. Medical science has not found the cure for the common cold. How in the hell can you refute the science that creates controversy as to the truth about AIDS and the HIV Virus. Science as we’ve all learned is not exact. This is why research is continued; findings are reported. While its ok to disagree, it is equally important to look at the whole picture absent the almighty dollar. It is critical that all information, good, bad, or indifferent be reported so that it sparks more research to answer the how and why. Money cannot be the motivator behind what gets reported and what doesn’t. The Bible says, the love of money is the root of all evil. It is heart breaking to have lost my sister at the tender age of 33. I miss her every day. I have not visited her grave or put flowers on it since we laid her to rest August 6, 2003. The pain is so deep. Almost three years later, just thinking of her brings tears to my eyes. She was an incredible person, not a lab rat. I am appalled and outraged at the attack Celia and Harper’s Magazine received because of an article. I sense that there was a bit of truth reported based upon the need to rebut the story and to discredit Dr. Duesberg. Nothing sparks hatred more than truth, perhaps more dumb docs. My sister was robbed of her life. Some quack doctors played God. Sterling will never know what a wonderful Mom he had. Sterling was robbed of the love only his mother could have showered on him. Jermal, her oldest son works even harder in school to make the memory of his Mom meaningful. He’s excelling and doing well. His mother would have been so proud. But you no nonsense “AIDS researchers” robbed her of that too. To Celia and Harper’s thank you. Thank you for caring enough to tell the truth. Thank you for dignity and respect. My family and I appreciate you bringing this to light. This story was not fiction. It was about a real person. It was about my friend, my confidant, my sister, Joyce Ann Hafford. Sincerely, Rubbie

 

Item #4: HIV Antibodies in Babies

Farber	All babies born to an HIV-positive mother are born positive, but most become negative within eighteen months.
Gallo	Farber states that all “babies born to HIV-positive mother are born positive but most become negative within 18 months.” Farber is clearly confused by the passing on of the mother's antibodies to the child, a natural mechanism that protects the child from infectious disease as its own immune system develops. These passively transferred antibodies are eliminated from the child's system within 18 months at most, usually rather sooner. If a child is infected with HIV, it produces its own antibodies, which persist. After 18 months, if the child still tests HIV-antibody positive, it is almost definitely its own antibodies that are producing the result. Furthermore, a PCR test for the presence of the virus itself can accurately determine a child's HIV status by about six weeks after birth.
RA	Farber’s statement is perfectly correct. Most babies of HIV-positive mothers become negative within 18 months. A noticeable percentage become HIV-negative after 18 months: “Of those [children] who will lose antibody [to HIV], an estimated 10.2% lose it after 15 months, and 2.5% after 18 months” (European Collaborative Study. Children born to women with HIV-1 infection: natural history and risk of transmission. Lancet. 1991; 337: 253-60). The use of PCR (’viral load’) is increasingly common for infants because of problems with antibody tests. However, these tests have never been approved for diagnostic purposes: “[The Roche Amplicor HIV-1 Monitor Test] is not intended to be used as a screening test for HIV or as a diagnostic test to confirm the presence of HIV infection” (Amplicor HIV-1 Monitor Test. Roche. 1999). “The VERSANT HIV-1 RNA 3.0 Assay (bDNA) is not intended for use as a screening assay for HIV infection or as a diagnostic test to confirm the diagnosis of HIV infection” (Summary of Safety and Effectiveness - Versant HIV-1 RNA 3.0 Assay. Versant. 2003 Jul 9) “The NucliSens HIV-1 QT assay is not intended to be used as a screening test for HIV-1 nor is it to be used as a diagnostic test to confirm the presence of HIV-1 infection.” (NucliSens HIV-1 QT. Organon Teknika. 2001 Nov 13).

 

Item #5: Problems with HIV Tests

Farber	HIV tests detect footprints, never the animal itself. These footprints, antibodies, are identified by means of molecular protein weights, and were limited to two in 1984, when the first test was developed and patented, but over the years expanded to include many proteins previously not associated with HIV. Like most Americans, Hafford thought that a single HIV-positive test meant that she “had” HIV—a surefire death sentence. But a majority of HIV-positive tests, when retested, come back indeterminate or negative. In many cases, different results emerge from the same blood tested in different labs. There are currently at least eleven different criteria for how many and what proteins at which band density signal “positive.” The most stringent criteria (four bands) are upheld in Australia and France; the least stringent (two bands), in Africa, where an HIV test is not even required as part of an AIDS diagnosis. The U.S. standard is three reactive bands. It has been pointed out that a person could revert to being HIV negative simply by buying a plane ticket from Uganda to Australia.
Gallo	In footnote one, Farber makes various false statements about HIV tests. She comments that HIV tests are not even required for an AIDS diagnosis in Africa. She also claims most HIV tests come back indeterminate or negative when redone. She supplies no references. Most people in the industrialised world, as well as many developing countries, have at least two different HIV antibody tests to confirm they are HIV-positive, as part of the HIV testing protocol. HIV tests are highly accurate. It is false that when most people are retested they test indeterminate or negative. Even the risk of a single HIV ELISA test giving a false positive is less than 1% with today's tests. HIV tests are required for an AIDS diagnosis in South Africa. They are also standard in Botswana, Kenya, Uganda and many other clinics throughout Africa. An AIDS diagnosis cannot be considered definitive without an HIV test. Farber's comment about hopping on a plane from Uganda to Australia to change HIV diagnosis is simply silly hyperbole.
RA	HIV not required for AIDS in Africa Farber is perfectly correct that an HIV test is not required in Africa. Quoting from the WHO’s 1994 AIDS Case Definition (the most recent WHO definition listed at who.int/hiv/strategic/surveillance/definitions/en): For the purposes of AIDS surveillance an adult or adolescent (>12 years of age) is considered to have AIDS if at least 2 of the following major signs are present in combination with at least 1 of the minor signs listed below, and if these signs are not known to be due to a condition unrelated to HIV infection. Major signs weight loss >= 10% of body weight chronic diarrhoea for more than 1 month prolonged fever for more than 1 month (intermmittent or constant) Minor signs persistent cough for more than 1 month generalized pruritic dermatitis etc. …Advantages of the WHO case definition for AIDS surveillance are that it is simple to use and inexpensive since it does not rely on HIV serological [antibody] testing. Limitations of this case definition are its relatively low sensitivity [i.e. it misses people with AIDS] and its low specificity [i.e. it is prone to false positive diagnoses] particularly with respect to tuberculosis… It is also not completely correct to note that HIV tests are required for an AIDS diagnosis in South Africa. It is true that HIV testing is performed, but to a much lower standard. A nationwide survey of South Africans [1], relied on two positive ELISA tests, while in North America generally three ELISA tests are performed, followed by a confirmatory test such as Western Blot. This will obviously result in more false positive test results. Another South African survey [2] used only a single ELISA test. Accuracy of HIV tests Since 1985 different sorts of biochemical tests have been licensed and used in laboratory-based clinical procedures known as ‘algorithms’. These algorithms are used by public health authorities to identify what have been thought of as antibodies to proteins of the human immunodeficiency virus (HIV). Case definitions by public health authorities (e.g. CDC) of the Acquired Immunodeficiency Syndrome (AIDS) refer to the results of these HIV antibody tests in order to define AIDS. These biochemical antibody tests were developed from the original laboratory algorithms first used to identify what were thought of as antibodies to HIV proteins. Two common antibody-based methodologies used today are the enzyme-linked immunosorbent assay (ELISA) and the Western blot (WB), both used for the screening of human populations for ‘HIV antibodies’. Manufacturer literature document that these tests produce false or indeterminate results because the interpretation of the test result is based solely upon the statistical probability of infection as opposed to the positive/negative isolation of a biological entity. In addition the biochemical laboratory identification in these tests of what are thought of as HIV proteins is known to be highly problematic, time-intensive and so requires ‘surrogate’ techniques. This is because direct isolation of the biological entity of any retrovirus in the laboratory is not possible. In other words, no HIV test has ever had its results correlated with detection of actual virus, so nobody actually knows if any positive HIV results are true positives. Across the world, public health officials use different algorithms for testing of humans for the presence of what are thought of as ‘HIV proteins’. These algorithms aim to balance test specificity and sensitivity by using variations of the original test methodologies and differing commercially available tests. However, they all are premised upon the health professional’s perception of the ‘exposure risk’ of the client/patient, which is determined during pre-test dialogue in the clinic: how the test subject is positioned by the professional as ‘high’/‘low’ risk within a hierarchy of exposure categories. This means that the results of these tests are not based upon the identification of any biological retroviral entity, or even the biochemical reaction in the laboratory, but they are based on interpretation of the laboratory test signal in relation to the client’s/patient’s perceived probability of infection. The interpretation of indeterminate results is problematic given the possibility of false results, which are ruled out by estimating the risk of exposure (‘window period’) and the seroprevalence in the ‘risk population’ of the test subject based on what ‘risk behaviour’ the subject discloses to the health professional or which the latter surmises during the clinic interview. Since 1985, experience with these test algorithms has shown that the interpretation of the test ‘result’ is not wholly ‘objective’ i.e. the interpretation of the test result is not determined by what happens in the laboratory because it relies upon classifying the test subject as being ‘at risk’ during pre-test dialogue rather than the biochemical signal reaction in the ELISA or WB. This sort of information is generally not known by many health professionals who do not understand how ‘HIV tests’ are conducted and the premise of probability upon which they are based. An example of problems with the tests comes from the 1980s, before the algorithms were fully standardized, at a time when intermediate results were still sometimes reported. The researchers studying a large low-risk population stated that “Although exact percentages were not routinely recorded and calculated, approximately 1% of all initial screening ELISA were reactive [positive], 50% of repeat [second] ELISAs were reactive, and 30% to 40% of first Western blot assays were reactive and diagnostic” [3]. Today, algorithms for HIV testing do not specify duplicate Western blot assays, so many false positives, perhaps still the majority of tests, go unrecognized. It is also important to note that standards vary around the world, especially for interpretation of the Western Blot ‘Confirmatory’ test. Eleven radically different interpretations have been documented for use in different countries and by different organizations.
Refs.	Shisana O et al. South African national HIV prevalence, HIV incidence, behaviour and communication survey, 2005. HSRC Press. 2005. Pettifor AE et al. Young people’s sexual health in South Africa: HIV prevalence and sexual behaviors from a nationally representative household survey. AIDS. 2005 Sep 23; 19(14): 1525-1534. Burke DS et al. Measurement of the false positive rate in a screening program for human immunodeficiency virus infections. N Engl J Med. 1988; 319(15): 961-4.

 

Item #6: Comparing Clinical Trial PACTG 1022 to HIVNET 012

Farber	On August 8, 2003, Jonathan Fishbein, who had recently taken a job as the director of the Office for Policy in Clinical Research Operations at DAIDS, wrote an email to his boss, DAIDS director Ed Tramont, alerting him that “there was a fulminant liver failure resulting in death” in a DAIDS trial and that it looked like “nevirapine was the likely culprit.” He said that the FDA was being informed. He was referring to Joyce Ann Hafford. Tramont emailed him hack, “Ouch. Not much we can do about dumb docs!” This email exchange came to light in December 2004, when AP reporter John Solomon broke the story that Fishbein was seeking whistle-blower protection, in part because he had refused to sign off on the reprimand of an NIH officer who had sent the FDA a safety report concerning the DAIDS trial that launched the worldwide use of nevirapine for pregnant women. The study was called HIVNET 012, and it began in Uganda in 1997.
Gallo	Farber switches from a discussion of PACTG 1022 to HIVNET 012 and omits to explain a critical distinction. Here Farber misleads in a way that is repeated throughout the remainder of the article. She confuses the short-course nevirapine-only regimen used to reduce MTCT with chronic treatment using nevirapine as one component of a combination of ARVs. Not a single life-threatening event related to short-course nevirapine has been recorded in mother or child in tens of thousands of such uses around the world. The nevirapine toxicity found in PACTG 1022 was in chronic treatment.
RA	In our opinion Farber quite neatly moves from a discussion of the trial that resulted in the death of one American woman to the Uganda trial of the same drug. Writing style is somewhat a matter of opinion, but the fact that both trials had serious problems with adverse events, and both involved the same drug, Nevirapine, surely is connection enough to allow them to both belong in the same magazine article.

 

Item #7: Are reports of PACTG 1022 Sinister?

Farber	The conclusion of the PACTG 1022 study team was published in the journal JAIDS in July of 2004. “The study was suspended,” the authors reported, “because of greater than expected toxicity and changes in nevirapine prescribing information.” They reported that within the nevirapine group, “one subject developed fulminant hepatic liver failure and died, and another developed Stevens-Johnson syndrome.” Stevens-Johnson syndrome is skin necrolysis—a severe toxic reaction that is similar to internal third-degree burns, in which the skin detaches from the body. Another paper, entitled “Toxicity with Continuous Nevirapine in Pregnancy: Results from PACTG 1022,” puts the results in charts, with artful graphics. A small illustration of Hafford's liver floats in a box, with what looks like a jagged gash running through it. Four of the women in the nevirapine group developed hepatic toxicity. As Terri Schiavo lay in her fourteenth year of a persistent vegetative state, and the nation erupted into a classically American moral opera over the sanctity of life, Joyce Ann Hafford's story made only a fleeting appearance—accompanied by a photo of her holding a red rose in an article that was also written by the AP's John Solomon. But soon a chorus of condemnation was turned against those who were sensationalizing Hafford's death and the growing HIVNET controversy to condemn nevirapine, which had been branded by the AIDS industry as a “life-saving” drug and a “very important tool” to combat HIV in the Third World.
Gallo	Farber reports on the publication of PACTG 1022 as if it is something sinister. In fact, its publication was standard scientific procedure. Furthermore, that nevirapine toxicity was reported in the paper is an indication of honestly conducted science that is inconsistent with Farber’s implications of some sort of cover-up. There is no logical comparison with the Schiavo case; Farber's analogy is bizarre and hard to understand.
RA	This appears to be more a critique of Farber’s writing style than anything else. It is a fairly straightforward description of the publication that admitted that there were serious consequences for several people in a US-based trial of Nevirapine. It is interesting to contrast the lack of interest over the Hafford death versus the highly publicized Terry Schiavo death watch. It may be possible to argue that the legal issues in the Schiavo case made it particularly compelling (as opposed to just Schadenfreude), but it is also possible to argue that Hafford should be seen as an icon for the many people who die in clinical trials. And it is true that the serious reactions of all six UK men in a recent clinical trial did get widespread press attention (see, for example, news.bbc.co.uk/1/hi/england/london/4807042.stm), so perhaps more attention is being drawn to this important issue.

 

Item #8: Comparing Clinical Trial PACTG 1022 to HIVNET 012

Farber	soon a chorus of condemnation was turned against those who were sensationalizing Hafford's death and the growing HIVNET controversy to condemn nevirapine, which had been branded by the AIDS industry as a “life-saving” drug and a “very important tool” to combat HIV in the Third World.
Gallo	Farber's repeats her mistake on p. 39 col. 3. Farber fails to inform her readers that she is switching back and forth between a discussion of chronic nevirapine use for treatment with short-course nevirapine for MTCT reduction.
RA	Farber is correctly noting that proponents of Nevirapine in the third world were worried that reports of fatal toxicity in the first world would dent the demand for this drug. Hafford was not an isolated case, the CDC had previously, in 2001, warned about fatal liver failure when this drug was used for post-exposure prophylaxis [1]. A journal report noted 30 cases of liver toxicity in HIV-negative people taking Nevirapine [2]. While data from one trial cannot be directly extrapolated to a different trial with a different regimen of the same drug, concerns about toxicity should certainly not be ignored. Adverse events will presumably be lower with a single dose but, given that another serious adverse effect of Nevirapine is hypersensitivity reactions, even a single dose could be a serious problem. The manufacturer warned in 2003 that “Severe, life-threatening skin reactions, including fatal cases, have occurred in patients treated with VIRAMUNE [Nevirapine]. These have included severe cases of SJS [Stevens-Johnson syndrome, pictures at www.sjsupport.org/pdf/SJS_factsheet.pdf], TEN [Toxic Epidermal Necrosis (skin death)], and hypersensitivity reactions characterized by rash, constitutional findings, and organ dysfunction.” [3]
Refs.	CDC. Serious adverse events attributed to Nevirapine regimens for postexposure prophylaxis after HIV exposures - worldwide 1997-2000. MMWR. 2001 Jan 5; 49(51): 1153-6. Patel SM et al. Serious Adverse Cutaneous and Hepatic Toxicities Associated With Nevirapine Use by Non-HIV-Infected Individuals. J Acquir Immune Defic Syndr. 2004 Feb 1; 35(2): 120-125. Guidelines for management of rash with Viramune (nevirapine). Boehringer Ingelheim. 2003 April.

 

Item #9: Is it Okay That the Elizabeth Glaser Pediatric AIDS Foundation Takes Money from the Nevirapine Manufacturer?

Farber	Front and center were organizations like the Elizabeth Glaser Pediatric AIDS Foundation, which extolled the importance of nevirapine. Elizabeth Glaser's nevirapine defenders apparently didn't encounter a single media professional who knew, or cared, that the organization had received $1 million from nevirapine's maker, Boehringer Ingelheim, in 2000. This was no scandal but simply part of a landscape. Pharmaceutical companies fund AIDS organizations, which in turn are quoted uncritically in the media about how many lives their drugs save.
Gallo	Farber points out that Elizabeth Glaser Pediatric AIDS Foundation (EGPAF) has taken money from Boehringer Ingelheim and implies this disqualifies them from commenting on the safety of short-course nevirapine. It is the function of the EGPAF, a registered charity, to prevent MTCT. The fact that the EGPAF has taken money from Boehringer Ingelheim does not disqualify it from commenting on the safety of nevirapine. The EGPAF is not selling nevirapine on behalf of Boehringer, but distributing it free of charge to those without access to it. Farber only mentions the EGPAF with respect to affirming the safety and efficacy nevirapine and links this to their Boehringer grant. But many organisations affirmed the safety and efficacy of single-dose nevirapine, including ones without financial connections to the pharmaceutical industry such as the World Health Organisation, the nobel peace prize-winning organisation, Medecins Sans Frontieres, and the Treatment Action Campaign. [This supposed error relies on a footnote (number 4) which notes that AIDS is defined differently in Africa.] It is true that as more was learnt about AIDS, the definition of the disease changed. There is nothing unusual in this; AIDS was only discovered in 1981. It is a testimony to scientific methodology that it only took a few years to discover its cause. An accurate diagnosis of AIDS, throughout the world, does require an HIV-positive test. While there are facilities in Africa which do not even have HIV tests (one of the cheapest components of the medical response to HIV), our knowledge of HIV in Africa is based on studies that have used HIV tests. (Incidentally, facilities that cannot offer HIV testing do not offer ARVs either.) We show later that numerous studies conducted in Africa have demonstrated that people with HIV have much higher morbidity and mortality than people without HIV. Also see Nicoll and Killewo (2000). 24
RA	Farber was not commenting so much on the appropriateness of the Glaser foundation taking drug company money, but on the lack of concern in the press that this might cause the organization to avoid criticism of its paymasters. AIDS foundations will only consider the morality of taking drug company handouts when they are called to account for this conflict of interest. While the mainstream media is becoming increasingly critical of the money-driven medical system in many areas, HIV/AIDS is an exception, apparently immune from criticism.

 

Item #10: The Definition of AIDS in Africa

Farber	Africa, as the news media never tires of telling us, has become ground zero of the AIDS epidemic. The clinical definition of AIDS in Africa, however, is stunningly broad and generic, and was seemingly designed to be little other than a signal for funding. It is in no way comparable to Western definitions. The “Bangui definition” of AIDS was established in the city of Bangui in the Central African Republic, at a conference in 1985. The definition requires neither a positive HIV test nor a low T-cell count, as in the West, but only the presence of chronic diarrhea, fever, significant weight loss, and asthenia, as well as other minor symptoms. These happen to be the symptoms of chronic malnutrition, malaria, parasitic infections, and other common African illnesses. (In 1994 the definition was updated to suggest the use of HIV tests, but in practice they are prohibitively expensive.) Even when HIV tests are performed, many diseases that are endemic to Africa, such as malaria and TB, are known to cause false positives. The statistical picture of AIDS in Africa, consequently, is a communal projection based on very rough estimates of HIV positives, culled from select and small samples, which are extrapolated across the continent using computer models and highly questionable assumptions.
Gallo	Footnote 4 states that AIDS is defined differently in Africa. It is true that as more was learnt about AIDS, the definition of the disease changed. There is nothing unusual in this; AIDS was only discovered in 1981. It is a testimony to scientific methodology that it only took a few years to discover its cause. An accurate diagnosis of AIDS, throughout the world, does require an HIV-positive test. While there are facilities in Africa which do not even have HIV tests (one of the cheapest components of the medical response to HIV), our knowledge of HIV in Africa is based on studies that have used HIV tests. (Incidentally, facilities that cannot offer HIV testing do not offer ARVs either.) We show later that numerous studies conducted in Africa have demonstrated that people with HIV have much higher morbidity and mortality than people without HIV. Also see Nicoll and Killewo (2000). 24
RA	The Gallo document is wrong to claim that HIV tests are needed for an AIDS definition. The World Health Organization’s 1986 ‘Bangui’ definition [1], updated in 1994 [2], states that HIV tests are not needed and that the definition can be based solely on common clinical symptoms: “For the purposes of AIDS surveillance an adult or adolescent (>12 years of age) is considered to have AIDS if at least 2 of the following major signs are present in combination with at least 1 of the minor signs listed below, and if these signs are not known to be due to a condition unrelated to HIV infection. Major signs weight loss >= 10% of body weight chronic diarrhoea for more than 1 month prolonged fever for more than 1 month (intermmittent or constant) Minor signs persistent cough for more than 1 month generalized pruritic dermatitis etc. …Advantages of the WHO case definition for AIDS surveillance are that it is simple to use and inexpensive since it does not rely on HIV serological [antibody] testing. Limitations of this case definition are its relatively low sensitivity [i.e. it misses people with AIDS] and its low specificity [i.e. it is prone to false positive diagnoses] particularly with respect to tuberculosis…” (our emphasis)
Refs.	WHO case definitions for AIDS surveillance in adults and adolescents. Wkly Epidemiol Rec. 1994 Sep 16; 69(37): 273-5. WHO/CDC case definition for AIDS. Wkly Epidemiol Rec. 1986 Mar 7; 61(10): 69-76.

 

Item #11: Does HIV, not Poverty, Predict Progression to AIDS in Africa?

Farber	Africa, as the news media never tires of telling us, has become ground zero of the AIDS epidemic. The clinical definition of AIDS in Africa, however, is stunningly broad and generic, and was seemingly designed to be little other than a signal for funding. It is in no way comparable to Western definitions. The “Bangui definition” of AIDS was established in the city of Bangui in the Central African Republic, at a conference in 1985. The definition requires neither a positive HIV test nor a low T-cell count, as in the West, but only the presence of chronic diarrhea, fever, significant weight loss, and asthenia, as well as other minor symptoms. These happen to be the symptoms of chronic malnutrition, malaria, parasitic infections, and other common African illnesses. (In 1994 the [WHO’s Bangui AIDS] definition was updated to suggest the use of HIV tests, but in practice they are prohibitively expensive.) Even when HIV tests are performed, many diseases that are endemic to Africa, such as malaria and TB, are known to cause false positives. The statistical picture of AIDS in Africa, consequently, is a communal projection based on very rough estimates of HIV positives, culled from select and small samples, which are extrapolated across the continent using computer models and highly questionable assumptions.
Gallo	Footnote 4 also states that AIDS happens to have the same symptoms as “chronic malnutrition, malaria, parasitic infections and other common African illnesses.” HIV, not poverty, predicts progression to AIDS in Africa. Of course, living in poverty increases the risk of acquiring HIV infection, because poor people have less access to information about how HIV is spread and how to avoid contracting this infection. Also, poor people, especially poor women, frequently have less power to negotiate the use of condoms. HIV-infected people living in resource-poor environments can progress more rapidly to AIDS and death because of their reduced access to health care and their diminished state of general health compared to individuals who reside in more affluent settings. As NIAID (2003) explains, the “diseases that have come to be associated with AIDS in Africa -such as wasting syndrome, diarrheal diseases and TB -have long been severe burdens there. However, high rates of mortality from these diseases, formerly confined to the elderly and malnourished, are now common among HIV-infected young and middle-aged people, including well-educated members of the middle class.”25 Sewankambo et al. (2000) is a study of nearly 20,000 people, both HIV-positive and HIV-negative in a Ugandan district. People with HIV were much more likely to get sick or die. Furthermore death rates in civil servants and the better-educated (i.e. not the poor) were higher than the general population. This was associated with HIV infection. 26 Statistics South Africa (2005) counted South African death certificates between 1997 and 2002 and found a 57% increase in mortality (only a small portion can be accounted for by improved death registration and population growth). Critically, most of this increase is accounted for in young adults, with the highest proportion of adult deaths in 2002 being 30-39 year olds. Child mortality has also risen dramatically. This is incompatible with poverty as the cause of AIDS, especially in a country where living standards improved to some degree (or at worst stayed the same) during the period studied. 27 Furthemore, some AIDS-related diseases, e.g. cryptococcal meningitis, are very rare in people without HIV, but very common in Africa in people with HIV. We provide further detail in the endnotes. 28
RA	The World Health Organization “Bangui” definition of AIDS [1] (see rethinkaids.info/GalloRebuttal/Farber-Gallo-10.html) does not require a positive HIV test and is based on very generic symptoms such as fever, cough, diarrhea and weight loss. Even so, the Sewankambo paper that the Gallo document cites as evidence that “HIV, not poverty, predicts progression to AIDS in Africa” and which does show a very high death rate associated with positive HIV tests also states that “only 56 out of 615 deaths (9.1%) met the WHO criteria [for AIDS].” [2] This means that positive HIV tests are correlated with sickness, but not necessarily with AIDS. This is easy to explain if there is a high rate of false positive HIV tests or if HIV is just a “passenger virus” transmitted by risky activities (such as injections with unsterile needles). The danger of interpreting HIV tests as reliable indicators of AIDS is that it persuades people to accept a fatal diagnosis, which is enough to kill some people, and it also persuades people to accept toxic AIDS drugs, where they are available, which will also kill some people.
Refs.	WHO case definitions for AIDS surveillance in adults and adolescents. Wkly Epidemiol Rec. 1994 Sep 16; 69(37): 273-5. Sewankambo NK et al. Mortality associated with HIV infection in rural Rakai district, Uganda. AIDS. 2000 Oct 20; 14(15): 2391-400.

 

Item #12: Are HIV Tests Widely Used in Africa?

Farber	In 1994 the [WHO’s Bangui AIDS] definition was updated to suggest the use of HIV tests, but in practice they are prohibitively expensive.
Gallo	Footnote 4 further states that HIV tests are prohibitively expensive in Africa. HIV tests are widely available across Africa. They are not prohibitively expensive for large numbers of people.
RA	A copy of the reporting form for AIDS cases in both South Africa and Uganda can be found at: aids-kritik.de/aids/SA/meldeformulare.htm. This shows that in South Africa one has to report whether or not an HIV test has been done in an Aids case (i.e. an HIV test is optional). In Uganda the Ministry of Health’s form does not even ask for an HIV test.

 

Item #13: Tropical Diseases and False Positive HIV Tests

Farber	Even when HIV tests are performed, many diseases that are endemic to Africa, such as malaria and TB, are known to cause false positives.
Gallo	Footnote 4 further states “many diseases that are endemic to Africa, such as malaria and TB, are known to give false positives.” Farber fails to supply a reference. The risk of a false positive HIV test in Africa, as elsewhere, is very small if the correct protocol is followed. Some HIV antibody tests have been tested in Africa and found to be very accurate. These are the ones generally used. For example, the Abbott Determine rapid test used widely in South Africa has a specificity of at least 98% (and in some studies has achieved close to 100%). When this test is combined with a second rapid test or an ELISA test to determine HIV status, the risk of a false positive is negligible. The contribution of TB and malaria to false positives on today's tests is also negligible. For examples of trials of HIV tests used in Africa and Brazil, see Sauer et al. (2000)29 , Phili et al. (2002)30 , Ferreira et al. (2005)31 , Koblavi-Dème et al. (2001)32 and Foglia et al. (2004)33 .
RA	There are several papers indicating that diseases common in tropical areas, including Africa, can cause false positive HIV tests, although not enough work has been done in this area: Leprosy, or contact with Leprosy patients: “Sera from 63.6% of leprosy patients and 23% of their contacts was repeatedly positive by HIV ELISA [which in Africa and England is enough for a diagnosis of HIV infection]” [1] Malaria: “The prevalence of malarial parasitaemia was 13% [in a serological survey of 250 outpatients in rural Zaire]. However, 72% of patients had antibodies against P falciparum [the malaria parasite]…The proportions of subjects positive in the ELISA test for HTLV-I, HTLV-II and HTLV-III [HIV] were 14%, 25% and 12%, respectively...When the titer [level] of antibodies against P falciparum was considered...this single factor dominated all others...If the human retrovirus reactivity observed in the ELISA tests is frequently non-specific among Africans, the causes of the non-specificity need to be clarified.” [2] Malaria: “We evaluated serum samples from a group of 12 patients with acute Plasmodium vivax infection [malaria] who lived in…southwestern Venezuela…Our second group, 12 patients with Plasmodium falciparum infection…None of the patients were receiving antimalarial drugs…and none belonged to any of the recognized AIDS risk groups or had any AIDS-associated disorders…3 of the patients with P. falciparum infection (25%) and 5 with P. vivax (41%) were found to be positive for HTLV-III/LAV [HIV] antivodies by [3 antibody test types]” [3] Unspecified: “the proportion of HTLV-III [HIV] seropositive patients was notably high among those with idiopathic splenomegaly [enlarged spleen with no known cause] and schistosomiasis [parasitic infection]…Among Kenyans, the Turkana have the highest and the [closely related] Masai have the lowest prevalence of antibodies against both viruses [HTLV-I and HTLV-III(HIV)]…the Turkana inhabit a desolate area of desert and scrub-brush and are the poorest and most isolated of the groups that we studied…the Turkana have many other parasitic and viral infections [apart from seasonal malaria], including one of the highest rates of hydatid [tapeworm] disease in the world and a high prevalence of hepatitis markers…In view of the high prevalence of HTLV-III antibody, AIDS illness might have been expected to be frequent, yet no cases have been documented in Kenya [to 1985]. We are aware of only 3 cases suspected of being AIDS-related…it is unlikely that AIDS-illnesses of the recognized varieties are occurring at a rate commensurate with the prevalance of antibody against HTLV-III” [4] Several Diseases: “The currently used laboratory based and rapid HIV-tests show intolerably high numbers of false positive results when used in developing countries. This is mainly due to interfering effects of diseases virtually absent in developed countries.” [5] Even if the error rate of these HIV tests was just 2% this would mean that, in a population where 10% of people are testing positive, it would mean that 8% were true positives, and 2% false, with no way to tell the difference.
Refs.	Kashala O et al. 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 lipoarabinomannan. J Infect Dis. 1994 Feb; 169: 296-304. Biggar RJ et al. ELISA HTLV retrovirus antibody reactivity associated with malaria and immune complexes in healthy Africans. Lancet. 1985 Sep 7; 2(8454): 520-3. Volsky DJ et al. Antibodies to HTLV-III/LAV in Venezuelan patients with acute malarial infections. N Engl J Med. 1986 Mar 6; 314(10): 647-8. Biggar RJ et al. Regional variation in prevalence of antibody against human T-lymphotropic virus types I and III in Kenya, East Africa. Int J Cancer. 1985 Jun 15; 35(6): 763-7. gaifar.com. 2004 Sep [accessed]. www.gaifar.com.

 

Item #14: African HIV/AIDS Statistics

Farber	The statistical picture of AIDS in Africa, consequently, is a communal projection based on very rough estimates of HIV positives, culled from select and small samples, which are extrapolated across the continent using computer models and highly questionable assumptions.
Gallo	Footnote 4 states “The statistical picture of AIDS in Africa, consequently, is a communal projection based on very rough estimates of HIV positives culled from select and small samples, which are extrapolated across the continent using computer models and highly questionable assumptions.” (1) Statistical estimates are not extrapolated across the continent, but on a per country basis. (2) Large samples of people with HIV have been taken in a number of countries including Kenya, Botswana, Uganda and South Africa. (3) South Africa's HIV/AIDS surveillance is arguably better than most industrialised countries, let alone developing countries. It comes from annual antenatal surveys, two countrywide household surveys, numerous small community surveys and death certificates. The most widely used computer model used to determine the size of South Africa's epidemic closely matches the prevalence calculated in the latest countrywide household survey. See ASSA (2005)34 and Shisana et al. (2005)35 . (4) It is true that estimates of AIDS in most African countries are imprecise, but there is evidence showing beyond reasonable doubt that the African HIV epidemic is massive. For a detailed rebuttal of the claim that HIV is not a serious epidemic in Africa see Geffen (2004)36 .
RR	Rodney Richards, an expert on HIV testing, and one of the founding scientists at biotech giant Amgen, has provided a detailed analysis of problems with South African AIDS statistics, at least when interpreted according to the HIV=AIDS=Death model. Some of its highlights are: “Farber’s further characterization of these [South African HIV] prevalence estimates as “very rough,” may be debatable, but certainly cannot summarily be characterized as either false or misleading.” “if we are to believe the results of these surveys, then we have to accept that HIV antibody prevalence among white South Africans dropped from 6.2% in 2002 to only 0.6% in 2005; representing an unbelievable 90% reduction” “the ASSA2003 model [that the Gallo document claimed “closely matches the prevalence calculated in the latest countrywide household survey”] overestimated prevalence among sexually active (age 15-49) coloureds, whites, and asians, by 63%, 171%, and 215%, respectively” “if it is indeed the case that CDR [Completeness of Death Registration] in rural SA was as low as 37% in 1997, and that it subsequently increased to 90% by 2002, this shift alone would result in a 143% increase in reported deaths” “the correlation between the observed increases in reported death at the provincial level (expressed as rates) and HIV prevalence as determined in the 1997 ANC survey is feeble at best” “relatively lower provincial death registration in 1996 predicts a remarkable 77% of higher subsequent increases in reported death from 1997-2002” “a critical analysis of the observed increases in reported death in SA over the past several years does not support the suggestion that these increases serve to validate HIV prevalence estimates”
RA	What are the statistics regarding AIDS and HIV infection in Africa? “I think it is time to start questioning some of the claims made by the Aids lobby. Their certainties are so fanatical, the powers they claim so far-reaching. Their authority is ultimately derived from computer-generated estimates, which they wield like weapons, overwhelming any resistance with dumbfounding atom bombs of hypothetical human misery. Give them their head, and they will commandeer all resources to fight just one disease.” Rian Malan, 2003 [1] Decline of AIDS and Genesis of HIV/AIDS When the term HIV/AIDS replaced AIDS in the late 1990s, it completely muddied the water. The rationale for transmuting AIDS into HIV/AIDS was never formally articulated. This change was facilitated when the US Centers for Disease Control (CDC) elevated the status of two laboratory results in its 1993 definition of AIDS to allow an otherwise healthy American with antibodies to HIV and fewer than 200 CD4 cells per microliter of blood to be defined as an AIDS case [2]. Solely on the basis of this provision of the 1993 definition, the number of new AIDS cases increased three-fold, literally overnight. (Figure 1) [3]. This new category, which was to become HIV/AIDS, destroyed the distinction between HIV and AIDS. The equation HIV=AIDS=disease=death that has been drilled into the public psyche since 1984 also made it easy for the AIDS orthodoxy to promote the new label HIV/AIDS. But why was there a need to replace AIDS with HIV/AIDS? When AIDS (defined by real diseases) is tracked and reported, the epidemic is shown to have essentially burned itself out throughout the world, including Africa (Figure 2), by the beginning of the new millennium. Instead of publicizing the good news, the CDC stopped reporting actual AIDS cases after 1997. The number of new cases had been dropping steadily since 1993 (Figure 3) [3]. Ever since, computer models have been cranking out apocalyptic numbers of an exploding pandemic of HIV/AIDS. The CDC keeps track of the number of new AIDS cases according to three definition categories, each of which expanded what constitutes AIDS: pre-1987, 1987 and 1993. The CDC’s rule is that the diagnosis of AIDS must be made according to the earliest definition that qualifies. This rule makes the dramatic increase in the proportion of new AIDS cases (now called HIV/AIDS) based on the 1993 definition even more striking. From 1994 to 1997 the proportions rose from 49 to 68% (Table 11, from page 17 of reference [3]). Manufacturing the African HIV/AIDS Pandemic The current HIV/AIDS pandemic is solely dependent on divining how many people around the world have antibodies that react with the so-called HIV tests. I say divining because over 95% of the computer-generated 40+ million people with “HIV/AIDS” have never been tested for antibodies to HIV, as most are poor Africans. Therefore, in order to generate the colossal African HIV/AIDS numbers, the AIDS orthodoxy extrapolates from results for HIV-antibodies in pregnant Africans [4-6]. These extrapolations are absolutely necessary to generating an ever-growing virtual pandemic of HIV/AIDS. It is generally accepted that South Africa has the best statistics in sub-Saharan Africa. Before 1998, two HIV-antibody tests had been performed for the South African surveys: one screening test and a confirmation test on the positive samples. The second test was skipped from 1998 onwards (except in Western Cape) even though richer countries usually require four tests to define someone as HIV-positive: an initial positive ELISA, at least one of two follow-up ELISA tests being positive followed by a positive Western Blot. The manufacturer of the HIV-antibody test that was used in these (see reference [4]) and earlier surveys, specifically warns that, “at present there is no recognized standard for establishing the presence or absence of HIV-1 antibody in human blood.” Furthermore, it also warns that “non-specific reactions may be seen in samples from some people who, for example, due to prior pregnancy...have antibodies to the human cells or media in which HIV-1 is grown for manufacture of the EIA” [7]. In other words the test, which may show false positive reactions in women with “prior pregnancy”, is being used in pregnant women without further confirmation or adjustment. This can explain why “Studies from seven African countries over the last 15 years show rates of HIV incidence during antenatal and/or post-partum periods exceeding what could be expected solely from sexual transmission” [8]. Yet, these problematic, unconfirmed results from pregnant women are then used to estimate the frequency of HIV in the general population [5] and eventually the whole of sub-Saharan Africa [6]. Reality Check Ultimately, any real pandemic, regardless of its name, would at some point be made obvious by a surge in disease and death, well-above normal levels. The question, then, is there evidence, independent of extrapolations and computer-generated numbers, showing extraordinary increases of disease and death? An ability to keep track of the annual number of deaths, irrespective of cause, is all that is needed to determine if something unusual is going on. Statistics South Africa (Stats SA) reports a constant growth in the population of South Africa from 38 million in 1994 to 43 million in 2001 [9, 10]. Furthermore, the rise in the number of deaths from all causes during the same period was also constant, growing as the population grows—but no faster (Figure 4). The latest antenatal screening survey in South Africa also failed to support the hypothesis that HIV is sexually transmitted [4] but instead confirms the conclusion of Brewer et al. that, “HIV is not transmitted by ‘sex’” [11]. The survey included testing pregnant women for syphilis and antibodies to HIV in order to see how the two diseases were correlated by geographical location and over time. But, there was no correlation. On the contrary, in 2000, KwaZulu-Natal, which is leading when it comes to HIV, has the lowest rate of syphilis in all provinces. Western Cape, on the other hand, had the highest rate of syphilis but the lowest HIV prevalence. Paradoxically, there is an inverse geographical correlation between syphilis and HIV (Figure 5) although both are said to be transmitted by heterosexual intercourse. An even more extraordinary result is the divergence over time between an increasing prevalence of antibodies to HIV and a declining rate of syphilis (Figure 6) [4]. This is also difficult to understand given the assumption that both are sexually transmitted. A 1999 study in Uganda produced similar results. The intention of the study had been to reduce HIV incidence by mass treatment of STDs with conventional antibiotics. The rationale behind the study was that reducing STDs (which was assumed to be a co-factor in the transmission of HIV) should reduce the transmission of HIV. However, the result of the study was paradoxical. While the investigators were very successful in significantly reducing STDs, their intervention had “no [effect] on incidence of HIV-1 infection...” [12]. The data from Thailand show that these inconsistent results are not peculiar to Africa. Even though Thailand is said to be severely hit by a heterosexually transmitted HIV-epidemic, we find, yet again, the same scenario presented by South Africa and Uganda. Bangkok has the highest rate of STDs but low HIV prevalence. Conversely, the so called Golden Triangle of northern Thailand has the highest rate of HIV but the second lowest STD morbidity of all regions. And, even within the different provinces of the Northern Region there is a negative correlation between HIV and syphilis [13]. The conclusion from these observations is obvious: HIV cannot be heterosexually transmitted. Given these and other impossibilities surrounding AIDS, President Thabo Mbeki convened the Presidential AIDS Advisory Panel in Pretoria, South Africa in May 2000 to answer basic questions. Many of the panelists were excited by the prospect of obtaining the very latest and best information and statistics on AIDS in South Africa. However, this was not to be. As stated in the Interim Report of the meeting released in March 2001: “The deliberations of the panel were at all times bedevilled by the absence of accurate and reliable data and statistics on the magnitude of the AIDS problem or even HIV prevalence in South Africa. Repeated requests for such data and statistics, failed to result in the provision of such data by either South African panellists or the officials of the Department of Health.” [14] So, where does one find the best statistics on AIDS in Africa, if not South Africa? Something Doesn’t Compute A perusal of the World Health Organization Global Health Atlas website (globalatlas.who.int/globalatlas/dataQuery/default.asp) allows one to query for the actual number of annual AIDS cases (not HIV/AIDS) from 1979 through 2001 for 167 countries. You can also ask for cumulative numbers for years 2001 and 2003 for 210 countries. You will find many curious bits of information in the WHO database. For example, the cumulative number of AIDS cases in the USA for 2001 and 2003 were identical: 806,157. If one is to believe this result, then there were no new AIDS cases in the USA between 2001 and 2003. The USA is not the only country so privileged. Robert Gallo’s four African countries all had unchanging totals —Kenya: 81,492, Botswana:10,178, Uganda:55,861and South Africa:12,825. Globally, the cumulative total number of AIDS cases as of March 27, 2006, reported on the WHO Global Health Atlas website was 2,965,292. The WHO has not updated this figure since 2003, which is interesting in itself. A likely reason for not keeping the database up to date is revealed by a simple plot of the annual number of globally reported AIDS cases for the period 1979-2001 (Figure 2A). Such a graph shows AIDS cases rising from insignificant numbers through the mid 1980s to a peak in 1995 (analogous with the CDC’s 1993 peak for the USA (Figure 3)), followed by a precipitous decline through 2001. The cumulative total for the entire world produced by this graph is 2.8 million through 2001. The cumulative total for sub-Saharan Africa is 1.1 million AIDS cases (Figure 2B). By the end of 2003, the total had climbed to only 1,15 million. According to the WHO database, Africa gained an average of just under 23,000 new AIDS cases per year. To get a feeling for the meaningfulness of these AIDS numbers, one must compare them to the population explosion Africa experienced during the quarter-century of AIDS. From 1980 through 2005, the sub-Saharan Africa gained 358 million people [15], equivalent to 1.3 times the population of the USA. However, as of March 2006, the WHO reported, as described above, a total of only 1.15 million AIDS cases (not HIV or HIV/AIDS). Even if all of those 1.15 million peopled died, their deaths due to AIDS would be difficult to detect in a background of 358 million new sub-Saharan Africans. It also needs to be mentioned that African AIDS-defining diseases are indistinguishable from conventional African morbidity and mortality [16]. The WHO’s tally of just under 3 million global AIDS cases spread over a quarter-century is much less alarming and useful to the AIDS orthodoxy than its computer generated 24 million to 48 million cases of HIV/AIDS for 2003 alone (figures obtained from the same WHO website above). The complete disconnect between the number of actual AIDS deaths compared to computer-generated numbers based on the HIV/AIDS model was eloquently documented by the revered South African author Rian Malan in his 2001 article “AIDS in Africa: in search of truth” [17]. Malan is not alone in his criticism of what he calls the AIDS lobby. Because of the many epidemiological and clinical differences between African AIDS and its American/European namesake, and because of the many uncertainties about the statistics on African AIDS [18] both the novelty of African AIDS and its relationship to American/European AIDS have recently been called into question by a number of others [18-25]. In conclusion, the computer generated cases of HIV/AIDS has transformed a disappearing AIDS epidemic, the real diseases and actual deaths, into a new global pandemic of hypothetical infections and virtual corpses.
Refs.	Malan R. Africa isn't dying of Aids. The Spectator 2003 December 13. Centers for Disease Control and Prevention. 1993 revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. Morb Mort Weekly Rep 1992,41(No. RR17):1-19. Centers for Disease Control and Prevention. U.S. HIV and AIDS cases reported through December 1997, Year-end edition. HIV AIDS Surveillance Report 1997,9:1-43. Makubalo LE, Netshidzivhani PM, Mulumba R, et al. Summary Report:NATIONAL HIV AND SYPHILIS SERO-PREVALENCE SURVEY IN SOUTH AFRICA. In. Pretoria, South Africa: Directorate: Health Systems Research, Research Coordination and Epidemiology; 2001. Ntsaluba A. National HIV and Syphilis Sero-Prevalence Surveyof women attending Public Antenatal Clinics in South Africa 2000. In. Pretoria, South Africa: Ministry of Health, Director-General for Health; 2000:13 pages. UNAIDS. 2004 report on the global HIV/AIDS epidemic: 4th global report. In: Joint United Nations Programme on HIV/AIDS. Geneva; 2004. Abbott Laboratories Diagnostics Division. Human Immunodeficiency virus type 1 HIVAB HIV-1 EIA. In. Abbott Park, IL: Abbott Laboratories; 1997. Gisselquist D, Rothenberg R, Potterat J, Drucker E. HIV infections in sub-Saharan Africa not explained by sexual or vertical transmission. Int J STD AIDS 2002,13:657-666. Statistics South Africa. Causes of death in South Africa 1997-2001. In; 2002. Statistics South Africa. South African Statistics 2000. In; 2000. Brewer DD, Brody S, Drucker E, et al. Mounting anomalies in the epidemiology of HIV in Africa: cry the beloved paradigm. International Journal of STD & AIDS 2003,14:144-147. Wawer MJ, Sewankambo NK, Serwadda D, et al. Control of sexually transmitted diseases for AIDS prevention in Uganda: a randomised community trial. Rakai Project Study Group. Lancet 1999,353:525-535. Chitwarakorn Aea. Sexually Transmitted Diseases in Asia and the Pacific. Region 10, Chiang Mai, Thailand: Ministry of Public Health, AIDS Division, HIV/AIDS Situation in Thailand; 1998. Secretariat for Thabo Mbeki. Presidential AIDS Advisory Panel Report. In. Johannesburg; 2001. Bureau of the Census. World population by region and development category: 1950-2025. In. Washington, DC: U.S. Department of Commerce; 2001. World Health Organization. Provisional WHO clinical case definition for AIDS. Weekly Epidemiological Records 1986,March, 7, (10):72-73. Malan R. AIDS in Africa in search of the truth. Rolling Stone 2001 November 22:70-72, 74-78, 80, 82, 100, 102. Fiala C. AIDS in Africa: dirty tricks. New African 1998:36-38. Shenton J. Positively False: exposing the myths around HIV and AIDS. London/New York: I. B. Tauris; 1998. Stewart GT, Mhlongo S, de Harven E, et al. The Durban Declaration is not accepted by all. Nature 2000,407:286. Gellman B. S. African President Escalates AIDS Feud. Washington Post 2000:Sect. A01. Fiala C, de Harven E, Herxheimer A, Kohnlein C, Mhlongo S, Stewart GT. HIV/AIDS data in South Africa. Lancet 2002,359:1782. Ross E. Sub-Saharan Africa, Kenyia and the Malthusian paradigm in contemporary development thinking. In: Reclaiming Knowledge for Diversity. Edited by Pimbert M: Routledge or Earthscan; 2003:in press. Gisselquist D, Rothenberg R, Potterat J, Drucker E. HIV infections in sub-Saharan Africa not explained by sexual or vertical transmission. Int J STD AIDS 2002,13:657-666. Hodgkinson N. AIDS: the failure of contemporary science. London, UK: Fourth Estate; 1996.

 

Item #15: Who Benefits from Clinical Trials?

Farber	By June 2004, the National Institutes of Health had registered 10,906 clinical trials in ninety countries. The size of these trials, which range from the hundreds to more than 10,000 people for a single study, creates a huge market for trial participants, who are motivated by different factors in different societies but generally by some combination of the promise of better health care, prenatal care, free “access” to drugs, and often—especially in the United States—cash payments. Participating doctors, whose patient-care profits have been dwindling in recent years because of insurance-company restrictions, beef up their incomes by recruiting patients.
Gallo	Farber complains about the growth of clinical trials and claims that everyone profits except the subjects. She also implies that only the poor and disadvantaged are used as subjects. No reference is supplied to support the view that subjects on the whole are not benefiting from clinical trials. Many well-off people participate in clinical trials. The claim that most subjects of clinical trials are put at greater risk than benefit is astonishing, and it certainly contradicts common sense. Not every clinical trial is conducted perfectly, particularly from the perspective of record-keeping. Some are poorly conducted, but the vast majority conform to strict, internationally accepted ethical guidelines and benefit the study subjects.
RA	“There is a clear duty to provide assessment and explanation with appropriate reservations about the preliminary state of evidence and the fact that it may change with more data. This is an obligation all too often honored only in the breach, especially when the possibility of a new treatment, however remote, is present. Understandably, those afflicted with a serious illness and their families grasp desperately at any suggestion of cure or amelioration. They often listen selectively. They tend to filter out the negatives and overestimate the potential benefits. Such subjects are exceedingly vulnerable and exploitable, all of which sharpen the obligation to provide evidence with ethical circumspection.” [1]. “Patients died prematurely in two failed clinical trials at Seattle’s Fred Hutchinson Cancer Research Center - experiments using drugs in which the center and its doctors had a financial interest. The patients and their families were never told about those connections, nor were they fully and properly informed about the risks of the experiment.” [2] Dr. Samuel Epstein noted in “The Politics of Cancer Revisited” (East Ridge Press, 1998) that “While entering a clinical trial may well sound attractive, particularly to patients with advanced cancer, the chances of any benefits are remote.” Dr. Ralph Moss, in testimony to the US Congressional Committee on Government Reform and Oversight, said “If you read the statements of the NCI [a branch of the NIH] they urgently appeal to cancer patients to join their clinical trials…However, as the President’s Commission for the Study of Ethical Problems in Medicine stated (in 1983), “Patients who are asked to participate in tests of new anticancer drugs” should “not be misled about the likelihood (or remoteness) of any therapeutic benefit they might derive.’ In fact there is little chance of therapeutic benefit to patients in such trials. Studies in both the United States and Japan have shown that only about 1% of patients in Phase I clinical trials have a complete response to the treatment, and only about 5% have any response at all.” And, just as in AIDS, the outcome known as “response” is just a surrogate marker, a shrinkage of a tumor by 50% or more sustained for at least a month, not an indication of a cure. With AIDS it is very difficult to know if a trial is benefitting the patients because there is no placebo arm to the trials. Without such a control group it is impossible to distinguish between the adverse effects of the drugs and the progression of AIDS. Who gets to judge? Well, usually the researchers. The following remarks from three different studies illustrate how serious adverse events and deaths are trivialized or made to disappear by blaming them on HIV instead of one of the study drugs: “Of the 59 serious adverse events reported in the first 56 days of life, those that occurred in four (1.4%) babies in the zidovudine group and in two (0.7%) babies in the nevirapine group were judged [our emphasis] to be possibly, but unlikely to be, related to study drug…Within the first 56 days of life, 22 babies had grade 3 anaemia (nine in the zidovudine group, 13 in the nevirapine group), with haemoglobin values ranging from 85–118 g/L. No case was judged to be serious or clinically important.” [3] “Of the 217 clinical adverse events reported among children, most were [judged to be] due to a known cause unrelated to study drugs…16 children (4%) had major birth defects, including 4 cardiac malformation cases, 4 cases of polydactyly, 3 talipes cases, and 1 case each of congenital diaphragmatic hernia, hydronephrosis, imperforate anus, genu recurvatum with a suburethral cyst, and hypospadia. 1 child each had Down syndrome, Ito nevus, and sickle cell anemia” [4]. “There were 5 serious adverse events [out of 8 participants!] including two deaths in the infants in cohort 1 [Nevirapine to mother only]. Only one of the five serious adverse events was thought by the investigators to be possibly, but not likely study drug related…In cohort 2 [Nevirapine to mother and child] there were 7 serious adverse events [out of 13 participants], including 2 infant deaths, although none were [judged by the researchers to be] related to the study drug.” [5]. None of these trials had a placebo arm control group to the trial, so there is no way of knowing what caused the deaths and serious adverse events.
Refs.	Pellegrino ED. The ethical use of evidence in biomedicine. Eval Health Prof. 1999 Mar; 22(1): 33-43. Wilson D et al. Uninformed consent: what patients at ‘The Hutch’ weren’t told about the experiments in which they died. Seattle Times. 2001 Mar 11-15. Guay LA et al. Intrapartum and neonatal single-dose nevirapine compared with zidovudine for prevention of mother-to-child transmission of HIV-1 in Kampala, Uganda: HIVNET 012 randomised trial. Lancet. 1999 Sep 4; 354(9181): 795-802. Mandelbrot L et al. Lamivudine-Zidovudine Combination for Prevention o