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Denying AIDS and the Rwandan Genocide?

04 June 2006

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An example of the dishonesty of Valendar Turner and at least one of Christian Fiala, David Crowe, David Rasnick, Etienne de Harven, Henry Bauer, Ken Anderlini, Kevin Corbett and Martin Maloney

by Nathan Geffen and Jeanne Bergman, PhD

This article builds upon an issue raised by Nathan Geffen, Nicoli Nattrass and Glenda Gray in a letter in Nature (Nature 441, 406, 25 May 2006).1 In places we copy directly from that letter without reference. It is reprinted after this article.

There are so many instances of AIDS denialists egregiously misrepresenting facts that one can only reach the conclusion that they are dishonest or incompetent. Incompetence probably underlies their persistent rejection of scientifically proven facts and erroneous, obsolete, and thoroughly debunked claims. But we recently came across an apparently deliberate misrepresentation of legitimate research findings so deplorably wrong that it deserves special mention.

We recognize the seriousness of charging with dishonesty Valender Turner (who, as far as we can ascertain, first made this misrepresentation) and, for reiterating and signing their names to his error, at least one of Christian Fiala, David Crowe, David Rasnick, Etienne de Harven, Henry Bauer, Ken Anderlini, Kevin Corbett and Martin Maloney. We would comfortably defend our accusation in a court of law, because it is with high probability a true statement in the public interest. Some of the denialists, of course, have already been shown to be dishonest in other respects. For example, David Rasnick has repeatedly misrepresented a prior temporary affiliation with the University of California, Berkeley, despite requests from the University that he desist from doing so.2

The deception at hand began with a letter by Valendar Turner, an active member of “The Perth Group” of HIV denialists, last year in Nature ("HIV drug remains unproven without placebo trial" Nature 435, 137; 2005).3 Turner wrote that without a placebo-controlled randomized trial, statements that the efficacy of single-dose nevirapine in reducing perinatal transmission has not been invalidated are unwarranted. He contrasted the HIV transmission rate of 13.1% reported in the HIVNET 012 study4 (which he notes “abandoned its placebo group... under pressure of complaints that the use of placebo was unethical”) and stated that the “HIVNET 012 outcome is higher than the 12% transmission rate reported in a prospective study of 561 African women given no antiretroviral treatment (J. Ladner, et al. J Acquir. Immun. Def. Syndr. Hum. Retrovirol. 18, 293-298; 1998).” Turner’s inference is clear: perinatal HIV transmission was no better, perhaps even worse, with antiretroviral treatment than without it.

Turner's point was then amplified by a group writing to defend denialist Celia Farber from searing criticisms by Gallo et al. (2006)5 of her infamous article6 in Harper’s Magazine (March 2006). Farber had quoted Turner's letter and written that he had “unpegged the core claim of NIAID and its satellite organizations in the AIDS industry regarding nevirapine’s “effectiveness”.7

The group of individuals listed above—Fiala, Crowe, Rasnick, de Harven, Bauer, Anderlini, Corbett and Maloney–repeated the Turner claims in their effort to defend Farber. Their document is sloppy and littered with errors and admissions, but that's beyond the scope of this article. Our concern here is that they wrote:

Turner is referencing an African study published in 1998 that stated that “Presence of HIV-infection was assessed in 158 children [of HIV-positive mothers]… Overall, 19 children were diagnosed as HIV-infected [12%, even though there was no access to antiretroviral therapy or other interventions]” (Ladner J et al. Chorioamnionitis and pregnancy outcome in HIV-infected African women. J Acquir Immune Defic Syndr. 1998 Jul 1; 18(3): 293-8).

(Fiala et al., 2006, brackets in the original)8

If it were true, a finding that only 12% of the children born to a group of untreated HIV-positive Rwandan women were themselves infected with HIV would be surprising. Of course, it would not refute the findings of the HIVNET 012 study, which was a randomized controlled study and has far greater empirical value than a retrospective comparison of two cohorts from completely different studies. Nevertheless, the argument raised by Turner and Fiala et al. appeared on the face of it to have some, albeit small, merit.

A rebuttal to Turner's letter was published in a subsequent issue of Nature9, but it did not mention our critical point: the claim made by Turner and echoed by Fiala et al. that the Ladner et al. study10 found a 12% prevalence rate for a cohort of HIV-positive women not taking antiretrovirals is a gross misrepresentation of what the study reported. It is true that Ladner et al. found a 12% prevalence rate in 158 children born to untreated HIV-positive women. But those 158 children were only a fragment of the full cohort born to 275 HIV-positive women. The authors did not and could not examine the full cohort for the simple reason that many women and children had been lost to follow-up. Some of these had probably died of AIDS.

Ladner et al. had enrolled 275 HIV-positive women (and 286 HIV-negative women) in the study between July 1992 and August 1993.11 The women were between 24 and 28 weeks gestation. The researchers determined the HIV status of 158 of the children of HIV+ mothers enrolled in the study by antibody testing them at 15 months or by PCR tests at 3 and 6 months of age. Why only 158 of them?

What Turner and Fiala et al. neglect to point out is Ladner et al.’s sentence immediately preceding the section quoted by Fiala et al. above: "Follow-up of the cohort was interrupted by the events of the Rwandan civil war." (Ladner et al., op cit., emphasis ours.)

This statement about the disruption of the Rwandan civil war, one of the greatest human tragedies in recent history, not only immediately precedes the Ladner et al. quotation used by Fiala et al.; it is the first sentence of that paragraph! And, lest the point be missed, Ladner et al. return to the problem later, noting again that “We do not know the HIV status of the entire sample of children born to HIV-infected mothers as a result of interrupted follow-up.”

It is immediately clear to anyone with a rudimentary background in statistics (or just some common sense) that they’re not comparing apples to apples here. The low 12% figure, seized upon by Turner, Farber and Fiala et al. to understate the rate of perinatal HIV transmission by mothers without access to nevirapine, is an artifact of war, of genocide, and of AIDS itself.

The Ladner et al. study enrolled 275 HIV-positive pregnant women. 13.1% of these pregnancies ended in still births and 7.5 % of the newborns died, for a total reduction to the cohort of 20.6%--that’s 57 children, leaving 218 available for follow up. Only 158 of these children were tested for HIV, and of these 19 (12%) were found to be HIV-positive 3, 6 or 15 months later.

What happened to the other 60 missing children?

Fifteen months is long enough for many HIV-positive children and their mothers to have died of AIDS. In a study conducted in Uganda between 1994 and 1998, Brahmbhatt et al. found that 30.9% of the children perinatally infected with HIV died before their first birthday, and 54% by their second (Brahmbhatt, H. et al. Mortality in HIV-infected and uninfected children of HIV-infected and uninfected mothers in rural Uganda. J Acquir Immune Defic Syndr 2006; 41:504-508).

In Ladner et al.'s study, some of the children were possibly killed in the war --women and children sick with AIDS would have been less able to escape to safety. The surviving sample of the initial cohort was not representative, but rather skewed in favor of HIV-negative children. The actual figure for perinatal HIV transmission was almost certainly much higher. (Brahmbhatt et al. found perinatal HIV transmission rates in Uganda of 20.9%.)

We are by no means criticizing Ladner et al. Their paper is well worth reading. It is competent and interesting science conducted in staggeringly difficult circumstances. It was not their intention to determine vertical HIV transmission rates in the absence of antiretroviral intervention. Rather, the primary purpose of their paper was to compare Chorioamnionitis and pregnancy outcomes in HIV-positive and HIV-negative African women. The 12% statistic was a detail they included while carefully repudiating its statistical value.

The failure of Turner and of at least one of Fiala et al. to acknowledge the interruption of the follow-up of the cohort is either dishonest or grossly incompetent. On balance of probabilities it is dishonest. Researchers with the skill and tenacity to find an incidental HIV transmission rate figure buried in a not very well known article are unlikely to have missed the sentence "Follow-up of the cohort was interrupted by the events of the Rwandan civil war." More than likely, Turner and at least one of Fiala et al. realised this fact would negate the point they were making and deliberately left it out. This is dishonesty.

Or perhaps the AIDS denialists also deny the Rwandan genocide took place?

We accuse Turner and at least one of Fiala et al. of dishonesty for this misrepresentation. We are prepared to accept that not all of them intentionally omitted the relevant fact. When co-authoring an article, one depends on one's co-authors' integrity; it is seldom possible to check everything the others contribute. So if Fiala et al. indicate who among them was responsible for this dishonesty, we will relieve the remaining authors from the accusation of dishonesty on this particular point. Valendar Turner, however, has no excuse. He was the sole author of the letter to Nature that first misrepresented the research. He looked for and found an article with a figure—12%—that, if he dishonestly concealed the intervening genocide that prevented follow-up, would allow him to make his case.


2. See Last accessed 3 June 2006.

4. This study tested a short-course of the antiretroviral nevirapine for mother-to-child transmission prevention of HIV. It found that administering a single dose of nevirapine to mother and a single dose to child “lowers the risk of HIV-1 transmission by nearly 50% during the first 14-16 weeks of life in breast-fed infants”. 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. Last accessed 4 June 2006.

11. The Ladner et al article’s abstract gives the numbers of HIV-positive women enrolled as 286 and HIV-negative women enrolled as 275. This is a reversal of the numbers provided elsewhere in the text, including in the statistical charts. We therefore assume the error is in the abstract.

HIV denialists ignore large gap in the study they cite

Nature 441, 406 (25 May 2006) | doi:10.1038/441406c; Published online 24 May 2006 Nathan Geffen, Nicoli Nattrass and Glenda Gray Sir: Valendar Turner, in Correspondence ("HIV drug remains unproven without placebo trial" Nature 435, 137; 2005), argues that there is no evidence for antiretrovirals reducing the transmission of HIV from mother to child. He points out that HIV transmission in people taking the antiretroviral drug nevirapine was 13.1% in the HIVNET 012 study in Uganda, whereas only 12% of women in a Rwandan study were found to have transmitted HIV to their babies in the absence of antiretroviral treatment. Despite a rebuttal in Correspondence by the authors of the Ugandan study, Brooks Jackson and Thomas Fleming ("A drug is effective if better than a harmless control" Nature 434, 1067; 2005), Turner's letter continues to be cited by AIDS denialists (for example, C. Farber Harper's Magazine 37–52; March 2006). The Rwandan study referred to by Turner enrolled 561 pregnant women, of whom 286 were HIV-positive. Of the children born to HIV-positive mothers, 158 were tested for HIV and 19 (12%, as Turner states) were found to be HIV-positive. Why were only 158 children assessed? The answer, conveniently ignored by the denialists, is that follow-up was interrupted by the events of the Rwandan civil war (J. Ladner et al. J. Acquir. Immun. Def. Syndr. Hum. Retrovirol. 18, 293–298; 1998). Given that this interruption was sufficiently lengthy for many HIV-positive children and their mothers to die of AIDS in the interim, the surviving sample of the initial cohort cannot be regarded as representative. The actual figure for HIV transmission was almost certainly much higher. Failing to acknowledge this important caveat to the study appears to us to be inconsistent with accepted academic standards.