The scientific evidence for HIV/AIDS

Debunking denialist myths

AIDS denialists claim that HIV does not cause AIDS, that the risks of antiretrovirals outweigh their benefits or that there is not a serious HIV epidemic in sub-Saharan Africa. This webpage explains why these views are wrong.

We have deliberately kept the refutations of these myths on this page short. Instead of providing detailed scientific notes, we usually summarise key scientific findings and then provide links to more detailed refutations for readers who are interested. Additional material will be added to this site over time, to debunk other AIDS denialist myths. We recommend you monitor the site on a regular basis. Currently it debunks the following myths:

  1. HIV does not cause AIDS
  2. AIDS among minorities in the United States and other industrialised countries is caused by recreational drug use
  3. Studies, in particular one conducted by Nancy Padian and her colleagues, show that HIV cannot be transmitted heterosexually
  4. AIDS in haemophiliacs is caused by Factor VIII, a clotting agent in donated blood for haemophiliacs, not HIV
  5. AIDS in Africa is another name for old diseases caused by poverty
  6. There is no serious HIV epidemic in Africa
  7. AZT causes AIDS
  8. Although antiretrovirals work now, AZT when used as a monotherapy in the late 1980s and early 1990s killed more people than it helped
  9. The Concorde trial showed that AZT causes AIDS, or at least that AZT's risks outweigh its benefits
  10. Antiretrovirals have not been tested in clinical trials
  11. The Ugandan HIVNET 012 trial that studied the efficacy of single-dose nevirapine for mother-to-child HIV transmission prevention was scientifically and ethically flawed such that its results are unreliable
  12. False positive HIV test results are likely in pregnant women
  13. Tests that measure HIV directly are meaningless because they only find dead virus particles
  14. AZT does not triphosphorylate and therefore cannot work
  15. HIV cannot be detected post-mortem

 

Myth #1: HIV does not cause AIDS

Fact: HIV has been shown beyond reasonable doubt to be the cause of AIDS.

There is an abundance of evidence showing HIV is the cause of AIDS.  With very few exceptions, the human immunodeficiency virus itself or antibodies to HIV are detected in people with AIDS. Studies of people who are HIV-positive show they are more likely to develop AIDS symptoms and more likely to die at younger ages than people without HIV. Scientists can now describe in great detail how HIV infection occurs and causes AIDS. For detailed explanations see:

Also see:

These are two historically important papers that showed that HIV is the cause of AIDS. See this paper by Robert Gallo and Luc Montagnier. It describes how the discovery was made in the early 1980s.

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Myth #2: AIDS among minorities in the United States and other industrialised countries is caused by recreational drug use

Fact: There is no evidence supporting the myth that AIDS in gay men and other minorities in the United States and other industrialised countries is caused by recreational drug use.

No published peer-reviewed study supports this theory. Alcohol use can disinhibit people so that they increase their risk of HIV infection (e.g. by not using condoms). Excessive alcohol use also increases the risk of people on highly active antiretroviral treatment (HAART) not adhering to their medication thereby leading to disease progression.

M.S. Ascher and team examined the drug use data of several research cohorts and found no correlation between drug use and AIDS. The graph below is from that study, Does drug use cause AIDS?, published in Nature in 1993.

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).

A 2008 study, Recreational drug use and T lymphocyte subpopulations in HIV-uninfected and HIV-infected men, examined this issue in the MACS cohort. The conclusion was that there are "no clinically meaningful associations between use of marijuana, cocaine, poppers, or amphetamines and CD4 and CD8 T cell counts, percentages, or rates of change in either HIV-uninfected or HIV-infected men".

Also see:

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Myth #3: Studies, in particular one conducted by Nancy Padian and her colleagues, show that HIV cannot be transmitted heterosexually

Fact: Studies actually show the opposite, i.e. that HIV can be and is transmitted heterosexually.

Nancy Padian responds to this myth in detail in this article.

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Myth #4: AIDS in haemophiliacs is caused by Factor VIII, a clotting agent in donated blood for haemophiliacs, not HIV

Fact: This has been disproved in numerous studies of haemophiliacs.

See Jon Cohen's explanation in Science, written in 1994. The Factor VIII myth is based on the fact that a high proportion of haemophiliacs exposed to Factor VIII developed AIDS in the US. But the explanation is as follows: "[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... [This is, of course, due to heterosexual transmission of HIV from the index cases to their sex partners.]

See detailed NIAID explanation debunking this myth.

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Myth #5: AIDS in Africa is another name for old diseases caused by poverty

Fact: AIDS in Africa is characterised by recorded increases in the prevalence of a number of illnesses in young adults.

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). The report has since been updated for 2003 (and part of 2004). The HIV-related mortality trends have become even clearer. 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. (Also see South African Medical Research Council report). For many more examples related to Africa see:

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Myth #6: There is no serious HIV epidemic in Africa

Fact: The HIV epidemic is extremely serious in many sub-Saharan African countries.

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 rebuttal of yet another Malan piece published in Noseweek in February 2007. Much more information confirming the seriousness of the HIV epidemic in many sub-Saharan African countries has been produced since the above rebuttal. Also see this Statistics South Africa report and this report by the South African Medical Research Council.

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Myth #7: AZT causes AIDS

Fact: AZT and other antiretrovirals helps people with AIDS live longer.

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. The table below shows how HAART (Highly Active Antiretrovial Therapy) has improved the probability of survival for people with HIV.

Source: Survival of Persons with and without HIV Infection in Denmark, 1995–2005

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Myth #8: Although antiretrovirals work now, AZT when used as a monotherapy in the late 1980s and early 1990s killed more people than it helped

Fact: Numerous studies have provided evidence that AZT used as a monotherapy in the late 1980s and 1990s prolonged lives.

PLEASE NOTE: OUR EXPLANATION SHOULD NOT BE READ AS AN ENDORSEMENT OF PROVIDING AZT AS A MONOTHERAPY. AZT SHOULD NOT BE USED AS A MONOTHERAPY EXCEPT IN SOME RESOURCE POOR FACILITIES FOR THE SOLE PURPOSE OF MOTHER-TO-CHILD TRANSMISSION PREVENTION AND WHERE SUCH FACILITIES CANNOT AFFORD TO PROVIDE BETTER OPTIONS.

This is a myth that is not only perpetuated by AIDS denialists. It is however unsupported by evidence and its perpetuation makes unnecessary concessions to denialists. In the late 1980s AZT monotherapy was of limited benefit and prescribed in doses that are now known to be too high and associated with more side-effects. Nevertheless, a number of studies demonstrated unequivocally that most patients who took AZT benefited. It is true that many people started AZT monotherapy too early and developed resistance. If they had delayed antiretroviral treatment until 1997 they would have had more treatment options, but this is a different issue that has no bearing on the question of whether people with HIV who took AZT monotherapy in the late 1980s and early 1990s did better or worse at the time than people at the same clinical stage of HIV who took nothing. NIAID's article AZT and AIDS states:

Uncontrolled studies have found increased survival and/or reduced frequency of opportunistic infections in patients with HIV disease and AIDS who were treated with AZT or other anti-retrovirals (Creagh-Kirk et al., 1988; Moore et al., 1991a,b; Ragni et al., 1992; Schinaia et al., 1991; Koblin et al., 1992; Graham et al., 1991, 1992, 1993; Longini, 1993; Vella et al., 1992, 1994; Saah et al., 1994; Bacellar et al., 1994). In the Multicenter AIDS Cohort Study, for example, HIV-infected individuals treated with AZT had significantly reduced mortality and progression to AIDS for follow-up intervals of six, 12, 18 and 24 months compared to those not taking AZT, even after adjusting for health status, CD4+ T cell counts and PCP prophylaxis (Graham et al., 1991, 1992). In addition, several cohort studies show that life expectancy of individuals with AIDS has increased since the use of AZT became common in 1986-87.

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Myth #9: The Concorde trial showed that AZT causes AIDS, or at least that AZT's risks outweigh its benefits

Fact: The Concorde trial showed no such thing.

This misunderstanding of the Concorde trial is a popular myth amongst AIDS denialists. Nowadays, AZT treatment is not given by itself to people with HIV/AIDS. Three (or sometimes four) drugs are used, and AZT is often a component of the cocktail due to its efficacy. But in the late 1980s, AZT monotherapy was the only HIV medication available. AZT alone was not a very good drug; it was given in large doses (much larger than today) and resulted in numerous side-effects. Nevertheless 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.

AIDS Denialists refer to the Concorde study as evidence for their belief that AZT's risks outweigh its benefits. But the Concorde study did not show this. 

The Concorde trial was the biggest AZT monotherapy study over the longest period of time. Its results actually show that AZT cannot be 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, the trial demonstrated that AZT was no more harmful than placebo and therefore cannot be the cause of AIDS. (This was not the purpose of the trial incidentally, but it follows from its results.)

The denialists misunderstand 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 --and this is the critical-- at this point the researchers were no longer comparing placebo against AZT.

As Brian Gazzard, one of the scientists involved in the Concorde trial, explained in an affidavit refuting an AIDS denialist initiated court case (the case was dismissed), 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 to be beneficial for people with AIDS. If the patients who took AZT immediately had progressed to AIDS faster than the placebo group then one could conclude that AZT in patients without AIDS symptoms is dangerous. But the study simply did not show this. Read Brian Gazzard's affidavit for a detailed explanation.

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  a 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, several 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.

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Myth #10: Antiretrovirals have not been tested in clinical trials

Fact: Every antiretroviral registered in South Africa and the United States as of July 2006 had been through a clinical trial which demonstrated its safety and efficacy.

We deal with this myth in detail here.

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Myth #11: The Ugandan HIVNET 012 trial that studied the efficacy of single-dose nevirapine for mother-to-child HIV transmission prevention was scientifically and ethically flawed such that its results are unreliable

Fact: The HIVNET 012 trial, albeit imperfect from a book-keeping perspective, was a soundly conducted trial. There is no evidence that its scientific results are incorrect. The criticisms of the ethics of the trial made by AIDS denialists are without foundation.

This myth is extensively debunked elsewhere on the aidstruth.org website. See:

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Myth #12: False positive HIV test results are likely in pregnant women

Fact: If proper protocol is followed, the risk of a false positive HIV result is extremely small.

Even in low prevalence populations, false positives are rare if proper protocols are followed. The Centre for Disease Control's Revised Recommendations for HIV Screening of Pregnant Women states: False-positive Western blot results (especially those with a majority of bands) are rare. For example, in a study that used a sensitive culture technique to test approximately 290,000 blood donors, no false-positive Western blot results were detected (75). In a study of the frequency of false-positive diagnoses among military applicants from a low-prevalence population (i.e., <1.5 infections/1,000 population), one false-positive result was detected among 135,187 persons tested (76). An HIV test should be considered positive only after screening and confirmatory tests are reactive. A confirmed positive test result indicates that a person has been infected with HIV. False-positive results when both screening and confirmatory tests are reactive are rare. However, the possibility of a mislabeled sample or laboratory error must be considered, especially for a client with no identifiable risk for HIV infection. HIV vaccine-induced antibodies may be detected by current tests and may cause a false-positive result (i.e., there is no HIV infection, only an immune response to the vaccine antigen). Persons whose test results are HIV-positive and who are identified as vaccine trial participants should be encouraged to contact or return to their trial site or an associated trial site for HIV counseling, testing, and referral (CTR) services.

Incorrect HIV test results occur primarily because of specimen-handling errors, laboratory errors, or failure to follow the recommended testing algorithm (76). However, patients might report incorrect test results because they misunderstood previous test results or misperceived that they were infected (77). Although these occurrences are rare, increased testing of pregnant women will result in additional indeterminate, false-positive, and incorrect results. Because of the significance of an HIV-positive test result, its impact on a woman's reproductive decisions, and the resulting need to consider HIV therapeutic drugs for both a pregnant woman and her infant, previous guidelines have emphasized that HIV test results must be obtained and interpreted correctly. In some circumstances, correct interpretation might require consideration of not only additional testing but also the woman's clinical condition and history of possible exposure to HIV. In recent years many HIV rapid tests that deliver results within 45 minutes have been developed. When two of these tests are used to measure HIV status they are very accurate (both sensitive and specific). In high HIV prevalence populations they provide an accurate and affordable means for pregnant women to determine their HIV status. See:

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Myth #13: Tests that measure HIV directly are meaningless because they only find dead virus particles

Fact: Viral load tests give an excellent indication of the amount of live virus in a person with HIV.

Studies show that viral load increases in most patients with HIV over time. Also, scientists as a matter of course can routinely take a sample of blood of a person with HIV and culture HIV from it in a laboratory. This would not be possible if the HIV in a person's body was already dead. For a technical explanation, read the NIAID article Course of HIV infection. This editorial in Annals of Internal Medicine reflects on the importance of viral load tests in HIV treatment.

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Myth #14: AZT does not triphosphorylate and therefore cannot work

Fact: AZT has been shown to work in clinical trials. There is evidence that AZT triphosphorylates.

This is an obscure myth perpetuated by the Perth Group of AIDS denialists. Triphosphorylation is a chemical process that must take place for AZT to work.

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 or is not fully understood is therefore secondary. Nevertheless, there is evidence that AZT can indeed be triphosphorylated both from laboratory experiments and from studies of the human body. Triphosphorylation is a chemical process that AZT undergoes in order to stop HIV from reproducing.

A detailed explanation of the evidence that AZT triphosphorylates is contained in David Back's affidavit in a South African court case (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 experiments  that have demonstrated that AZT triphosphorylates, studies such as CHARM have detected triphosphorylated AZT in the human body.

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Myth #15: HIV cannot be detected post-mortem

Fact: HIV can be detected post-mortem with a high degree of accuracy.

This is very important because deceased tissue donors need to be tested to ensure that tissue recipients are not infected with HIV. See:

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