This is an archive of the Treatment Action Campaign's public documents from
December 1998 until October 2008. I created this website because the TAC's
website appears unmaintained and people were concerned that it
was becoming increasingly hard to find important documents.
The menu items have been slightly edited and a new stylesheet applied to the site. But none of the documents have been edited, not even for minor errors. The text appears on this site as obtained from the Internet Archive.
The period covered by the archive encompassed the campaign for HIV medicines, the civil disobedience campaigns, the Competition Commission complaints, the 2008 xenophobic violence and the PMTCT, Khayelitsha health workers and Matthias Rath court cases.
[THIS WEBPAGE IS STILL BEING DEVELOPED.]
AIDS denialists claim that HIV does not cause AIDS or that there is not a serious HIV epidemic in sub-Saharan Africa. This webpage debunks their arguments. It will soon also debunk some other pseudo-scientific theories about HIV, including the myths that condoms don't protect against HIV transmission and that most HIV transmission in Africa is due to contaminated hospital equipment. While some of these myths were once plausible theories, they are now contradicted by such a large body of evidence that continuing to propose them is pseudo-scientific.
We have deliberately kept the refutations of pseudo-scientific myths on this page short. Instead of providing detailed scientific notes, we summarise key scientific findings and then provide links to more detailed refutations for readers who are interested.
There is arguably more evidence showing that HIV is the cause of AIDS than other virally caused disease.
The Evidence that HIV Causes AIDS
The Relationship Between the Human Immunodeficiency Virus and the Acquired Immunodeficiency Syndrome
Equal Treatment Issue 19: Science of HIV
NIAID Resources on HIV-AIDS Connection
Not a single study supports this theory.
As explained in an NIAID document:
"Observational studies of HIV-infected individuals have found that drug use does not accelerate progression to AIDS (Kaslow et al., 1989; Coates et al., 1990; Lifson et al., 1990; Robertson et al., 1990). In a Dutch cohort of HIV-seropositive homosexual men, no significant differences in sexual behavior or use of cannabis, alcohol, tobacco, nitrite inhalants, LSD or amphetamines were found between men who remained asymptomatic for long periods and those who progressed to AIDS (Keet et al., 1994). Another study, of five cohorts of homosexual men for whom dates of seroconversion were well-documented, found no association between HIV disease progression and history of sexually transmitted diseases, number of sexual partners, use of AZT, alcohol, tobacco or recreational drugs (Veugelers et al., 1994)."
Kaslow RA, Blackwelder WC, Ostrow DG, Yerg D, et al. No evidence for a role of alcohol or other psychoactive drugs in accelerating immunodeficiency in HIV-1-positive individuals. A report from the Multicenter AIDS Cohort Study. JAMA 1989;261(23):3424-9.
Coates RA, Farewell VT, Raboud J, Read SE, et al. Cofactors of progression to acquired immunodeficiency syndrome in a cohort of male sexual contacts of men with human immunodeficiency virus disease. Am J Epidemiol 1990;132(4):717-22.
See Jon Cohen's excellent explanation in Science, written in 1994.
The Factor VIII myth derives its only evidence from the fact that a high proportion of haemophiliacs exposed to factor VIII developed AIDS in the US. But this was traced to the fact that "[r]etrospective tests of the U.S. blood supply have shown that, in 1978, at least one batch of Factor VIII was contaminated with HIV" (NIAID document).
The NIAID document further states:
"Among HIV-seronegative patients with hemophilia A enrolled in the Transfusion Safety Study, no significant differences in CD4+ T cell counts were noted between 79 patients with no or minimal factor treatment and 53 patients with the largest amount of lifetime treatments ... ";
"In a report from the Multicenter Hemophilia Cohort Study, the mean CD4+ T cell counts among 161 HIV-seronegative hemophiliacs was 784/mm3; among 715 HIV-seropositive hemophiliacs, the mean CD4+ T cell count was 253/mm3 ...";
"In another study, no instances of AIDS-defining illnesses were seen among 402 HIV-seronegative hemophiliacs treated with factor therapy or in 83 hemophiliacs who received no treatment subsequent to 1979 (Aledort et al., 1993; Mosely et al., 1993).";
"In addition to the evidence from the cohort studies cited above, it should be noted that 10 to 20 percent of wives and sex partners of male HIV-positive hemophiliacs in the United States are also HIV-infected ..."
See detailed NIAID explanation debunking this myth.
Numerous studies in Africa have shown that HIV infection predicts higher disease and death rates. While poor people have greater exposure to HIV and are more likely to progress to AIDS faster once infected with HIV, there is no evidence that poverty is the cause of AIDS.
Here are two examples of the evidence that HIV is the cause of AIDS in Africa:
A study in Rakai, Uganda disproves that poverty is the cause of AIDS. The study looked at nearly 20,000 people and found a much higher death rate among HIV+ people. Furthermore, the HIV-related death-rate was higher among better-educated and well-off people.
A count of death certificates in South Africa from 1997 to 2002 showed a 57% rise in deaths that cannot be explained by population growth or improved death registration. While in 1997, most adults who died were between the ages of 60 to 79, by 2002 most adults who died were between the ages of 20 to 44 (see Statistics South Africa report on mortality). This cannot be explained by poverty, because (1) economic conditions in South Africa have not changed drastically enough to explain this sudden rise in adult mortality (on the contrary, the social wage in South Africa has increased during this time) and (2) if it had, we would expect to see a much higher rise in deaths among the elderly. The only plausible explanation of the increase in adult mortality in South Africa is HIV (see MRC report).
For many more examples related to Africa see:
The Evidence that HIV Causes AIDS
Equal Treatment Issue 19: Science of HIV (page 2)
Rebuttal of Rian Malan
Errors in Celia Farber's article in Harper's Magazine, March 2006
This myth was perpetuated by Rian Malan in articles that appeared in the Spectator and Noseweek (a South African magazine) at the end of December 2003.
For a list of studies showing high HIV prevalence in Africa, see the appendix to the Rebuttal of Rian Malan. Read the main text of the rebuttal of Malan for a detailed explanation of why his arguments are wrong.
Also see this Statistics South Africa report and this report by the South African Medical Research Council.
In the first AZT trial on people with AIDS symptoms, known as BW 002, 19 patients out of 137 on placebo died and 1 patient out of 145 on AZT died. The AZT patients did better on a range of scores including quality of life. (ref)
In another randomized placebo-controlled study known as ACTG 016, the efficacy of AZT in reducing disease progression in symptomatic people with CD4 counts of 200 to 500 was again demonstrated. No benefit was found for people with CD4 counts above 500. (ref)
Furthermore, numerous observational studies of AZT used in clinical practice have demonstrated its efficacy. (ref)
The myth that AZT causes AIDS is rebutted here in more detail.
This misrepresentation of the Concorde trial is perpetuated by a number of AIDS denialists, particularly Anthony Brink.
Nowadays, AZT treatment is not given by itself to people with HIV/AIDS. Three (or sometimes four) drugs are used. But back in the late 1980s, AZT monotherapy was pretty much all that was available. AZT alone was not a great drug; it was given in large doses (much larger than today) and resulted in numerous side-effects. But clinical trials demonstrated unequivocally that it was much better than placebo for people with symptoms of AIDS and CD4 counts less than 500.
In the first AZT trial on people with AIDS symptoms, known as BW 002, 19 patients out of 137 on placebo died and 1 patient out of 145 on AZT died. The AZT patients did better on a range of scores including quality of life.
In another randomized placebo-controlled study known as ACTG 016, the efficacy of AZT in reducing disease progression in symptomatic people with CD4 counts of 200 to 500 was again demonstrated. No benefit was found for people with CD4 counts above 500.
Denialists refer to the Concorde study as evidence for the AIDS denialist belief that AZT's risks outweigh its benefits. But the Concorde study most definitely did not reach this conclusion. It is true that it was the biggest AZT monotherapy study over the longest period of time. But it showed unequivocally that AZT is not the cause of AIDS. Concorde only examined people with HIV WITHOUT symptoms of AIDS. It compared two strategies: Approximately half the trial participants took AZT immediately and the other half took placebo UNTIL they developed AIDS. Once patients progressed to AIDS, they were unblinded from the trial and given AZT. The participants taking AZT immediately had slower disease progression in the first year, but this dissipated with time resulting in no statistical difference in progression to AIDS. Since a large, approximately equal, number of participants in both arms progressed to AIDS, it clearly shows that AZT was no more harmful than placebo and therefore cannot be the cause of AIDS.
The denialists misrepresent the following about the Concorde trial: In a long-term follow up of the Concorde patients those who deferred AZT treatment until they got AIDS were less likely (slightly, but statistically significantly) to die than those who took it immediately. But at this point the researchers were no longer comparing placebo against AZT.
As a scientist involved in the Concorde trial explained in an affidavit rebutting AIDS denialist Anthony Brink in a court case which Brink pulled out of, Concorde was not testing whether AZT was better than placebo; this was already known. It was only trying to determine whether AZT should be taken before one developed AIDS symptoms. It concluded that one should not.
If the patients in the placebo arm stayed on placebo and never took AZT when they got AIDS, then a comparison would have been possible (and we can conclude from the trials described above that such hypothetical patients would have done very badly). But this is not what happened: patients on placebo indeed started AZT treatment when they developed AIDS because AZT had previously been shown unequivocally to be beneficial for people with AIDS.
Also, if the patients who took AZT immediately progressed to AIDS faster than the placebo group then one could conclude that AZT in patients without AZT symptoms is dangerous. But the study simply did not show this.
We now know why taking AZT as a monotherapy before developing symptoms of AIDS was an unsuccessful strategy. Patients taking one antiretroviral develop a strain of HIV resistant to the virus in very short time (a few months on average). Consequently the drug stops destroying HIV and patients then experience the side-effects without the benefits. Then when they do eventually get AIDS, the drug no longer has a useful effect. With today's standard of triple-drug therapy, resistance takes, on average, a few years to develop. When this happens, patients have to switch to a new antiretroviral cocktail. The current medical consensus is that treatment should still be deferred until a CD4 count of less than 350 or an AIDS-defining illnesses.
An analysis of over 50 randomised placebo-controlled clinical trials by Rachel Jordan and her colleagues in 2002 demonstrated just how beneficial antiretroviral treatment is. Their analysis included 15 trials comparing AZT to placebo, including Concorde. They showed that patients taking one antiretroviral (i.e. AZT) were 30% less likely to progress to AIDS or death than patients taking placebo. Patients taking two antiretrovirals were 40% less likely to progress to AIDS or death than patients taking one antiretroviral. Patients taking three drugs were also 40% less likely to progress to AIDS or death than patients taking two. In other words: three drugs are better than two drugs which are better than one drug which is better than no drugs. Why, if antiretrovirals are poisonous, does taking more of them results in better clinical outcomes?
We think he perpetuates it to try to intimidate people by using difficult to understand biological terms. There's no need to be intimidated; he's wrong and he has been shown to be wrong in a court case in South Africa (case: 1894/2001). That he continues to perpetuate this myth demonstrates his dishonesty.
Triphosphorylation is a chemical process that is necessary for AZT to work. But AZT has been proven to work in clinical trials as well as studies of cohorts in real-world settings. Whether the mechanism for how it works is understood or not is therefore secondary. Nevertheless, AZT does triphosphorylate and it has been shown to triphosphorylate both in laboratory experiments and in the human body.
Triphosphorylation is simply a chemical process that AZT must undergo in order to stop HIV from reproducing.
A detailed explanation of the evidence that AZT triphosphorylates is David Back's affidavit in the South African court case 1894/2001.
Here is a very simple explanation based on Back's affidavit:
HIV reproduces by entering CD4+ T-cells and then using the reproductive machinery of the cell to reproduce itself. When HIV enters the CD4 cell, it must convert its RNA to DNA (see pages 4 and 5 of Equal Treatment Issue 19 or the BBC for a detailed explanation). An enzyme called reverse transcriptase is key to this process. AZT works by interfering with the DNA chain produced by reverse transcriptase and stopping the chain from growing. Once this happens, the virus is unable to continue its reproduction process.
AZT must be converted to what is known as its triphosphorylated form inside cells if it is to work. This triphosphorylated form is known as AZTTP. The action of the virus's reverse transcriptase enzyme actually inserts AZTTP into the growing viral DNA being produced from the virus's RNA. Once this happens, the viral DNA can grow no further and the viral reproduction process stops.
Besides laboratory studies that have demonstrated that AZT triphosphorylates, the CHARM study examined the intracellular phosphorylation of AZT and found that AZT does indeed triphosphorylate.