Chapter 2

2.1 Introduction

Most of the participants agreed that HIV exists, but not all acknowledged that it causes AIDS. Prof Duesberg reminded the panel that he had studied retroviruses for 30 years; and had elucidated their genetic structure, as well as the complexity of their genome and its three genes. He had also analysed the composite proteins, including the glycoproteins, which are the basis for the HIV test. (Note: p24 used in most diagnostic tests is not a glycoprotein). Intrigued by claims that retrovirus can cause disease in humans, he had started research in this field. In his experience, retroviruses do not kill the cells they invade but are latent passengers in humans and animals. He pointed out that 16 years and 16 billion dollars later, not a single HIV-positive patient had been cured. Two hundred thousand Americans get chain terminators every 6 hours, he said, and they are even given to pregnant women. He added that people with antibodies to HIV should have protection against HIV disease, since vaccines protect by inducing the production of antibodies. However, scientists find only antibodies in HIV-positive patients, rather than the virus itself. Furthermore, the virus replicates rapidly yet tends to cause disease only 10 years after infection, compared with other viruses, which cause disease within 5–10 days.

Dr Giraldo informed the panel that he started studying immune deficiency in 1965. He was convinced that the AIDS epidemic was worse than what the people who assert HIV as its cause believed. The levels of immune deficiency in Africa were increasing and had been increasing since 1974/1975, which preceded the recognition of AIDS by almost ten years. His preoccupation with AIDS arose out of a concern that the assertion that HIV was the cause of AIDS masked the catastrophe of AIDS and prevented politicians and governments from dealing with the real catastrophe and its real causes.

Both Prof Duesberg and Dr Giraldo do not subscribe to the causal link between HIV and AIDS. They do, however, believe that AIDS does exist, caused by factors other than HIV. There were, on the other hand, panellists such as Dr Rasnick who argued very consistently that AIDS does not exist and that AIDS would disappear instantaneously if all HIV testing was outlawed and the use of anti-retroviral drugs was terminated.

Those panellists who do not subscribe to the notion of HIV causing AIDS posed the following questions as key to the deliberations of the panel:

  • Does HIV cause AIDS?
  • Is AIDS contagious?
  • Is AIDS sexually transmitted?
  • Do the anti-HIV drugs do more harm than good?

2.2 Does HIV cause AIDS?

Dr Williamson gave a presentation that affirmed that HIV causes AIDS. It is a retrovirus belonging to the lentivirus family of these RNA (ribonucleic acid) viruses. Its genome consists of the following genes: gag, pol, env, nef, tat, vpr, vpu, vif. Like other retroviruses, it utilises the enzyme reverse transcriptase to produce DNA (deoxyribonucleic acid) within the host cell from the template of viral RNA. This DNA is then inserted into the host cell’s genome. She reminded everyone that there are two types of HIV: HIV-1 and HIV-2; but that HIV-2 is much less common and is clustered in various geographical areas of the world such as West Africa. She displayed a phylogenetic tree of the various subtypes of HIV-1 that have been well characterised and sequenced and also showed a slide of an electron micrograph of the virus by Hans Gelderblom (1997). She further alluded to the Simian Immune Deficiency Virus (SIV) that causes AIDS in some monkeys.

There was a body of opinion expressed in the panel that 'purification' of a virus, as well as electron micrographs of the 'pure' virus was essential to answering the question as to whether a particular virus exists or not. According to Drs de Harven and Turner, HIV has never been 'purified' and no electron micrograph of the 'pure' HIV ever published.

2.2.1 Visualisation and Isolation of the Virus Visualisation of HIV

Dr Turner in a presentation to the panel referred to the first description of the human immune deficiency virus by the groups of Montagnier and Gallo (1983). He described how Prof Montagnier 'supposedly purified' the retrovirus by running culture material from AIDS patients through sucrose density gradients. One of the three proteins extracted from this purified material reacted with sera from AIDS patients, and was later 'claimed' to be HIV p24 – a protein that is unique to HIV.

Dr Turner then went on to explain that in virology it is usually considered essential to take an electron micrograph of the gradient-purified material to prove that it contains retroviral particles. All of the 'supposed' electron micrographs of HIV published since the mid-1980s were from cell culture and never from a patient. The first electron micrograph of a gradient-purified HIV from a patient was only published 14 years later in March 1997 in the journal Virology by Gelderblom’s group at the Koch Institute. Unfortunately, the Gelderblom article did not present immunoreactivity evidence to confirm that what had been visualised was indeed HIV. The second electron micrograph was from the US National Cancer Institute. The latter electron micrograph does not possess particles that are typically retroviral in morphology; nor does it meet the specific morphology of a particular retrovirus. Furthermore, independent data indicate that the proteins labelled p24 and p18 have been found in a variety of uninfected human tissue using monoclonal antibodies to these ‘HIV proteins’. ‘Thus if gradient purified infected material consists of the same proteins as uninfected material and does not contain retroviral particles and is not pure, then it is difficult to see how this material can be called ‘purified HIV’, Dr Turner argued. This series of arguments was supported by several contributions from Dr de Harven who insisted that nobody has ever demonstrated by electron microscopy a single retroviral particle in the blood of a patient supposedly having a very high viral load count.

Furthermore, Dr Turner claimed that Prof Montagnier in a 1997 interview had said that he had not purified his 1983 virus and had been unable to find any particles with morphology typical of retroviruses in his gradient-purified material. Dr Turner concedes that regardless of where the proteins come from, AIDS patients certainly have antibodies that react with these proteins and these reactions correlate with having AIDS or developing AIDS or being at risk for AIDS. In spite of this, there appears to be a need to utilise a ‘gold standard’; which would involve relating the antibody test to viral isolation.

Prof Montagnier stated that in 1983 there was so little virus in the supernatant harvested from the first patient’s culture that no virus could be visualised in the electron microscope even after pelleting. Moreover, the sucrose gradient used to purify the virus would have altered its morphology. Therefore, the evidence for a retrovirus was only indirect, namely, reverse transcriptase activity; p25 antigen associated with the peak of reverse transcriptase activity at the density of 1.155 – 1.16 in the sucrose gradient; cross reactivity of the p25 antigen with that of equine infectious anaemia virus (another lentivirus); and transmissibility of these characteristics from the initial cell culture to lymphocyte cultures of blood donors showing no antibody against p25. He further stated that it remains very difficult to isolate infectious HIV from peripheral blood lymphocytes of asymptomatic patients since at this stage the virus is almost exclusively located in the hyperplastic lymph nodes. Subsequent work done by his group and many other groups working on the subject makes untenable the contention that HIV does not exist. Dr Morris elucidated further that HI viral material has been visualised on dendritic cells using in situ hybridisation techniques.

Dr Morris pointed out that it was still difficult to visualise the virus in peripheral blood in spite of high viral loads. She asserted, however, that visualising the virus is not really necessary since there were other equally acceptable ways of 'seeing' the virus including PCR, p24 antigens and viral culture. She further argued that it would hardly be possible to culture an organism that was not found in peripheral blood in the first place. She also indicated that purifying HIV from blood is really not relevant in terms of validating ELISAs. Thus, while it may be difficult to visualise HIV in peripheral blood, it is extremely easy to see it in lymph nodes that are the major site of viral replication. In the light of the above, she argues that Dr Turner’s insistence on withdrawing the ELISA test was inconsistent, especially when he admits that these tests in fact do correlate with AIDS. Dr Giraldo also accepted the epidemiological correlation between AIDS and positive ELISA and Western Blot tests. He stressed, however, that his difficulty lay in the conclusion that positive ELISA and Western Blot tests resulted from patients being infected with HIV. Isolation of HIV

By contrast, Prof Montagnier further stated that HIV could be readily isolated from peripheral blood lymphocytes (after in vitro activation) of patients at the full-blown stage of AIDS. This was indeed the case of the virus isolated by his group from patient LAI who had full blown AIDS with Karposi’s Sarcoma. The virus that was isolated from both the blood and the lymph node biopsy of this patient became the prototype for all HIV-1-antibody testing. Dr Williamson pointed out that isolating HIV from peripheral blood is still difficult because of interference by plasma proteins. Dr De Harven was not convinced by the 'difficulty' argument stating that it had been routine for him in his training to isolate other retroviruses from the blood of leukaemic mice.

Dr de Harven pointed out that the retroviral markers that are protein in nature are non-specific because the virus has not been isolated and the proteins being measured could be cellular in origin. Tests reliant on the detection of p24 are therefore not reliable. According to Dr de Harven, it is of no surprise that tests reliant upon immunoprecipitation of these markers, (i.e. ELISA and Western Blot), are not specific either as over 70 medical conditions unrelated to AIDS frequently test positive. He asserted that epidemiological studies of transmission were therefore based on the scientific fallacy of "virological studies based on viral markers in the absence of viral particles".

Dr Turner insisted that in order to determine the specificity of an antibody test, a viral load test or a viral burden test for HIV infection, it is essential to use a gold standard, which in this case is isolation of HIV from infected individuals. This, he asserted, should not be difficult to establish in South Africa.

2.2.2 PCR (Polymerase Chain Reaction) and ELISAs

As already stated above, some panellists, including Dr de Harven, concurred that there is not one single report in the entire medical literature in which a correlation has been established between high viral load measured by PCR of AIDS patients and the observation of HIV particles by electron microscopy. According to him, the best experts in the field concur that this essential correlation has never been made. Dr de Harven went on to stress that (1) any epidemiological studies based on ELISA or Western Blots would have to be fundamentally re-appraised; and (2) that following up AIDS patients with PCR measurement of viral load is, in his opinion, scientific nonsense.

Furthermore, there were repeated assertions by some panellists that Dr Kary Mullis, who won the Nobel Prize for developing the PCR, has cautioned that the PCR is not an acceptable method for measuring viral load. It was also argued that the PCR is not a test for virus per se but could be totally non-specific and therefore not identify HIV. In contrast Dr Williamson argues that one can directly detect the virus by PCR, virus culture and p24 antigen assays. She emphasised that the PCR was an acceptable method of specifically identifying HIV. The evidence for this, according to Dr Williamson, derives from the fact that the PCR test is based on very specific primers that are short stretches of DNA. When designing a PCR test, a data search is performed to ensure that the stretch of DNA identified is absolutely specific for HIV. PCR does not amplify random pieces of DNA - they might be small stretches of DNA, but they are highly specific. In further support of this, Dr Makgoba stated that the data he collected showed that all PCR tests performed locally are concordant with the available serology; and all serological tests are as good as international standards.

Dr Giraldo accused the proponents of the theory that HIV causes AIDS of attaching a lot of value to PCR amplification of fragments of nucleic acids because of their inability to isolate the complete HIV particles even from patients at the height of the disease. Furthermore, PCR is not quantitative because it is not reproducible - repeat amplifications of the same sample delivering different results. Prof Montagnier concurred that the PCR test was not very quantitative. However, Dr Morris presented data showing that virus could be quantitated using PCR and that this quantitation was of prognostic value.

Dr Lane pointed out that the ELISA is a screening test to detect whether someone might be infectious and is not a diagnostic test for HIV. However, a combination of the ELISA with a Western Blot provides a very accurate method of diagnosing HIV infection. Dr Giraldo did not understand how two tests that were individually not diagnostic could be the basis of a diagnosis when combined. Reference was made to the following statements made by the manufacturers of kits used for ELISA, Western Blot and PCR tests:

  • "ELISA testing cannot be used to diagnose AIDS, even if the recommended investigation of reactive specimens suggests that antibodies to HIV are present" and "Specimens found to be repeatably reactive by Abbott HIV AB HIV-1/HIV-2(rDNA) EIA must be investigated by additional more specific supplementary tests"
  • "Do not use this kit as the sole basis of diagnosing HIV-1 infection"
  • "The 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"

Furthermore, Dr Fiala cautioned that the reality in most countries other than the USA and in Europe forces them to use only ELISA or rapid tests meaning that their AIDS statistics are only derived from 'diagnostic tests' acknowledged by everyone to be inadequate.

Prof Montagnier explained, that the panel of sera which the ELISAs use for calibration are seroconversion sera, from people who have just started producing HIV antibody. Also, multiple tests are used because the kits are validated against false positive controls.

Dr Duesberg remarked that two million young people are tested each year for HIV antibodies when they are screened for the US Army. One in a thousand tests positive but there has never been any report of any developing AIDS in the 12–15 years that these tests have been performed. These assertions were contested by Dr Gayle who argued that data existed which contradicted what Dr Duesburg was claiming. Dr Duesberg remarked upon a paper describing a subset of AIDS patients who were antibody positive but PCR negative.

2.2.3 Clinical and Laboratory Evidence of Causation

Opinion was divided as to whether HIV causes AIDS.

Dr Williamson presented evidence that HIV is necessary and sufficient to cause AIDS but that cofactors increase the risk. She asserted that:

  • All patients diagnosed as having AIDS have HIV, but someone with HIV does not necessarily have to develop AIDS
  • Cofactors may increase the rate of transmission of HIV; or the rate of progression to AIDS; but cannot in themselves cause AIDS
  • HIV is transmitted sexually
  • SIV, a virus closely related to HIV, causes AIDS in monkeys
  • HIV levels in blood measured by viral load predict the chances of transmission of HIV; as well as progression, as does the level of CD4 cells and HIV-1 specific cytotoxic T-cells.
  • Lowering the amount of HIV in an infected individual reduces the rate of progression to AIDS
  • HIV is the pathogen that causes AIDS, and is not an innocent bystander

Dr Morris described how the onset of HIV infection in South Africans is accompanied by HIV-1 specific cellular responses such as cytotoxic T lymphocyte cell responses. In addition one can detect the virus by PCR and p24 antigen assays. Low CD4 counts are extremely rare in people without HIV. A single factor ¾ HIV ¾ predicts whether someone will develop AIDS.

Extensive epidemiological evidence has shown that the detection of a number of AIDS cases in countries is preceded by the detection of HIV antibodies in the population.

There are a large number of reports that have shown that transmission of HIV results in AIDS, and a number of examples where it has been proven, by characterising the virus in both the donor and the recipient, that transmission has occurred. Haemophiliacs who developed AIDS all received HIV-contaminated blood whereas haemophiliacs who did not receive contaminated blood did not develop AIDS. Accidental infections of researchers and healthcare workers have resulted in reduced CD4 counts in these individuals and the subsequent development of AIDS. HIV infected mothers may transmit the virus to their children, and paediatric AIDS is always associated with HIV.

Dr Morris presented evidence to show that HIV is not an innocent bystander but a pathogenic virus that destroys the immune system. This is known both from laboratory data as well as from what happens in an HIV infected person. She posed the following as certainties:

  • HIV infects and destroys CD4 T-cells and these are precisely the cells that are depleted in a person with AIDS
  • HIV destroys the architecture of the lymph nodes and the result is that follicular dendritic cells are unable to trap the virus, resulting in a spillover of the virus into the blood
  • HIV causes cells to fuse and form giant cells, and people that have these syncytia-inducing viruses have a faster progression to AIDS
  • In HIV infected persons, cells show what is called apoptosis or programmed cell death, as well as anergy, which means that they are unable to respond to other antigens.
  • HIV also stimulates a number of specific immune responses, for example cytotoxic T-lymphocytes (CTL) as well antibodies, and some of these also contribute to the pathogenesis of the disease.

She described a study by Mellors that demonstrated that in those HIV-positive individuals with the highest viral load, 62% of them had developed AIDS after five years. In those that had the lowest viral loads, only 8% had developed AIDS after five years. This viral load stays fairly constant during the long asymptomatic phase of infection, but it can fluctuate. Factors such as immune activation caused by opportunistic infections can increase viral loads. In addition the use of anti-retroviral drug therapies reduces the viral load which subsequently reduces the risk of developing AIDS.

Some individuals are classed as rapid progressors. They develop the disease very quickly and these individuals have very high viral loads that do not decline as they would in most persons – a decline in viral load due to the induction of specific immune responses. Rapid progressors show a precipitous drop in CD4 cell counts and the acquisition of symptoms. However, there are some individuals who have been infected for up to 20 years and show very low viral loads and very stable high CD4 counts. These are called long-term non-progressors.

Prof Montagnier averred that HIV can reduce the number of CD4 cells and destroy the immune system; but only some strains can directly kill the CD4 T-lymphocytes. There are however more indirect ways of killing T-cells and we know that most of the cells that are not infected die of apoptosis.

The opponents of the HIV/AIDS hypothesis described the assertion of AIDS as an infectious, viral and transmittable syndrome as based on a set of beliefs and myths and not on scientific facts. They argued strenuously to refute the HIV/AIDS hypothesis and posted numerous references on the Internet site to support their stance. They advanced various arguments and references that would explain why HIV was either not implicated at all in AIDS or was at best a passenger virus to the disease. These would also explain why it is possible to have HIV-negative AIDS patients. Prof Duesberg explained that the PCR test typically identifies only 1 in a 1 000 or, at most, 1 in 100 cells, as being infected with HIV, and, in some patients, the virus is not found at all. In the case of a true pathogenic infection of a virus (for instance, hepatitis virus), every liver cell would be infected.

Dr Papadopoulos-Eleopoulos claimed that she had at least 15 references where the evidence shows that HIV does not destroy the CD4 cells. In fact, she said, even Dr Anthony Fauci says that the decrease in CD4 cells is only apparent and is due to down-regulation of the CD4 cells and not due to their destruction.

Dr Lane corrected the statement attributed to Dr Fauci who was on record as having said that HIV can down-regulate CD4 expression and that HIV destroys CD4 cells. Dr Lane reported that his laboratory has demonstrated reproducibly that HIV "chews up CD4 T-lymphocytes". He invited the South African government to send researchers to his laboratory to witness this phenomenon and learn how the experiments are conducted.

Dr Duesberg pointed out that part of Koch's postulate states that the virus should be present in the course of disease in amounts corresponding to a disease. To which statement Dr Morris responded by illustrating that HI viral load correlated with the risk of developing AIDS. Drs Williamson and Gayle also added that a number of cases existed where Koch’s postulate was fulfilled.

Dr Duesberg was puzzled why, in the case of the three laboratory workers who contracted HIV disease through treating patients, the cases had not been written up in medical journals, as this would have been an opportunity to fulfil Koch’s postulate of causation by a microbe.

He also gave the example of Kaposi’s Sarcoma occurring in homosexual young men who were HIV-negative, caused, he claimed, by inhalation of nitrates.

Dr Bialy asserted that the case of Kimberly Bergallis, who was reported to have died after contracting HIV from her dentist, was actually a case of AZT (azidothymidine) poisoning. Dr Bialy asserted that the replicatory behaviour of HIV during the so-called ‘latent period’ and its sporadic changes in titre during the natural history of the disease were typical of a passenger virus.

2.2.4 Evidence from Animal Models

Dr Williamson then covered evidence from animal models. She explained that one can clone the entire genome of SIV, a virus that is a close relative of HIV, insert this into a plasmid and then inject this into macaques. The macaques then get a viraemia and they develop antibodies against SIV. Subsequently they experience a reduction of CD4 T-lymphocytes and the development of AIDS. This progression of disease mimics what happens in humans. According to Dr Williamson, this is clear evidence that SIV, a virus closely related to HIV, causes AIDS with no cofactors present.

Dr Rasnick proposed treating chimpanzees that had been inoculated a long time ago with blood from AIDS but never developed the disease, with the same anti-retrovirals now given to human patients. He was certain that these chimpanzees would develop AIDS because of the drugs.

2.2.5 Epidemiological Evidence

Prof Abdool-Karim quoted epidemiological evidence that HIV causes AIDS. The South African Demographic and Health Survey (SADHS) shows a reversal in mortality trends in South Africa, and a study from King Edward VIII Hospital in Durban show that the two-year fatality for children infected with HIV is almost 60%. The infant mortality rate has been shown to be more than double in HIV-positive children versus HIV-negative children at Chris Hani Baragwanath Hospital in Soweto. Data collected at the King Edward VIII Hospital shows that case fatality rates over the last four years have increased from 4.5% to 22.6%.

Dr Bialy mentioned the foolish challenge given to Dr Duesberg when he delivered the graduate speech at the Albert Einstein College of Medicine to inject himself with HIV if he were so sure that it did not cause AIDS. He recommended instead a "series of easily undertaken, immediately do-able, epidemiological studies" to prove or disprove once and for all that HIV causes AIDS. He also pointed out that epidemiological associations could not be used to demonstrate causality.

Despite over 700 000 patients in the USA being treated, there is no example of doctors and researchers having contracted AIDS from exposure to HIV-positive patients, claimed Dr Duesberg. Dr Gayle, who stated that she would be happy to provide information on the fact that there has been transmission to healthcare workers both in the US as well as in other continents refuted this contention.

Dr Stewart observed that in the USA and Europe AIDS was spreading only in very well-defined risk groups who were mainly homosexual men, their female partners who were consorts to bisexual men, and also in some groups of drug addicts. The plain fact was that it was spreading only in well-defined groups where behaviour and lifestyle was a predominant feature. Epidemiological information to date would not support any hypothesis that assumed that there was a single exclusive microbial cause of AIDS. "It is a fact that the passage of time has shown beyond all doubt that in the USA and Europe, AIDS is a disease that is not spreading in the general population by heterosexual transmission of HIV or anything else, although that may be a marker, but it is continuing to occur in the original risk groups."

2.3 Alternative hypothesis on the cause of AIDS

The panellists who do not subscribe to the notion of HIV causing AIDS presented various alternative theories and hypotheses on the cause of AIDS.

2.3.1 The Chemical AIDS Hypothesis

Dr Duesberg believes that the ‘chemical AIDS hypothesis’, and not HIV, explains all aspects of AIDS in the USA, Europe and Africa. The steady rise in AIDS cases is more in keeping with toxic causes as an infection would be expected to produce a bell-shaped curve with decline due to spontaneous immunity and deaths. Furthermore, infections would be expected to affect people randomly, rather than the selectivity shown by AIDS. Also, viral infections are specific causing only one syndrome and not over 30 AIDS-defining conditions. Dr Morris countered by stating that the steady rise in AIDS cases is not incompatible with HIV as the cause of AIDS because of the long period between infection and the onset of disease. Concerning the selectivity of AIDS, she explained that the sexual transmission of HIV meant that the virus will only be transmitted to sexually active individuals, and will not affect people randomly. Prof Duesburg suggested that the panel perform a study in which 100–200 patients, identified as having AIDS according to the Bangui definition, have their actual antibody status assessed.

Several panellists, including Drs Rasnick and Giraldo, supported the Chemaids hypothesis. They explained that it takes 10 years of exposure to toxins (such as recreational drugs, irradiation and AZT and possibly vitamin deficiency) to cause AIDS in the USA and Europe; whereas in Africa poverty, malnutrition and parasitic and tropical diseases were probable triggers of AIDS; which explains why AIDS in Africa is roughly equally distributed between the sexes.

Dr Bialy felt that the chemaids hypothesis alone was not sufficient to explain AIDS in Africa but that factors such as the biological parasitic burden that Africans experience in terms of multiple infections, etc over long periods of time is most definitely a contributor to the chronic immunodeficiencies that Africans experience.

2.3.2 The Immunotoxicological Hypothesis

The proponent of the immunotoxicological model (Dr Giraldo) listed five groups of stressors that can destroy the immune system - chemical stressors, physical stressors, biological stressors, mental stressors and nutritional stressors. The immunosuppression caused by these stressors can lead to AIDS even in people who are HIV-negative. The members of the panel who subscribe to HIV as the cause of AIDS accepted the suppression of the immune system by the stressors listed above. They did, nevertheless, point out that immunosuppression due to HIV is very different from toxin-related immunosuppression.

2.3.3 The Oxidation Hypothesis

Dr Papadopoulos-Eleopoulos suggested that oxidising agents could lead to immunosuppression and cause AIDS.

2.4 The involvement of cofactors (or risk factors) in AIDS

In a paper entitled 'AIDS pathogenesis: Alternative views', Prof Root-Bernstein advances several theories that may elucidate the relationship between HIV infection and what are termed cofactors. The interaction between these may explain the nature of the epidemic in different parts of the world.

The usage of the term 'cofactor' was, however, strongly opposed by some members of the panel, particularly the Perth Group, on the grounds that this term implies the existence of a primary factor and that this primary factor is HIV. They argue that HIV cannot be the primary factor since its existence has not been proven. Proof of the existence of the virus can only be obtained by isolation of the virus, which has not yet happened. Instead, these panel members asserted that the elements commonly called 'cofactors' are the primary factors that cause AIDS in the absence of any requisite HIV infection. A more neutral term to accommodate factors involved in AIDS without denoting the primacy of HIV as a cause of the disease was 'risk factors'. Therefore 'cofactor' is used in this chapter only in the context of proponents of HIV as the cause of AIDS.

2.4.1 Involvement of cofactors in HIV-causes-AIDS Hypothesis

The paper by Prof Root-Bernstein articulated three theories on the primary cause of AIDS where cofactors may or may not be required: Theories that link cofactors to the cause of AIDS by HIV

(a) Theory A: The HIV-only theory

The implications of HIV-is-both-necessary-and-sufficient theory of AIDS causation are that everyone is at equal risk of HIV infection and AIDS. Everyone exposed to an equal dose of HIV should have an equal chance of chronic infection. Everyone infected with HIV should progress to AIDS at the same rate. The only way to stop the progress of AIDS would be to stop HIV (Weiss 1993; Ho 1996).

Though Prof Montagnier is convinced that HIV plays a central role in the cause of AIDS, he found it difficult to explain, on the basis of the HIV-only-theory, why the AIDS epidemic was restricted to male homosexuals and intravenous drug users in the USA and Europe but has a heterosexual profile in countries of the South. Dr Sonnabend was another proponent of the HIV-causes-AIDS hypothesis who believed that issues of poverty and malnutrition were more important in the development of AIDS than the mainstream scientific establishment was currently acknowledging.

(b) Theory B: The cofactor-promoted HIV theory

This theory is based on the premise that, in addition to the fact that HIV is necessary for the development of AIDS, the rate of development of AIDS following HIV infection may be determined by the presence or absence of specific cofactors. These cofactors may be other viral, bacterial or parasitic infections, malnutrition, sexually transmitted diseases, TB or anything else that could have a profound effect on the immune system. It is well established experimentally that HIV infection requires that a potential T-cell host be in an activated or stimulated state and that many of these cofactors can achieve such activation.

(c) Theory C: The cofactors-required theory

A second version of the cofactor theory argues that HIV is necessary but not sufficient to cause AIDS. According to this theory, in the absence of cofactors, HIV is neither able to infect people nor to replicate within individuals once infection has occurred. Thus, healthy individuals are unlikely to become infected with HIV in the first instance; and HIV-infected individuals who can eliminate existing cofactor risks may be able to drive the infection into latency. Like the cofactor-promoted theory, the rate of progression to AIDS will be determined by cofactor presence, but, since cofactors are necessary and not just modulators, the elimination of cofactors should be as effective at stopping AIDS as is the treatment of HIV.

Many cofactors induce the production of cytokines, immune suppression and immune depression independent of HIV. Many of these cofactors induce immune system cells to express the receptors required by HIV for the infection of cells. Cofactors that need to be considered strongly

I. Allergenic cofactors

The interplay between HIV infection and infections such as TB, mycoplasma, Human Herpes Simplex Virus 8 (HHV-8), cytomegalovirus (CMV), Human T-cell Leukaemia Virus II (HTLV-II), hepatitis B, chancroid, and other sexually transmitted diseases is significant due to the concurrent burden imposed on the immune system.

  1. The relationship between TB and HIV has been of concern to health professionals, especially because HIV infection has increased the number of identified cases of TB. Active tuberculosis infection also increases the rate of progression from HIV infection to AIDS. A proposed mechanism for the increased rate of immune deterioration has been proposed by Placido et al.. (1997), who showed that viable M. tuberculosis increases the rates of apoptosis of alveolar macrophages in AIDS patients. Apoptosis was not increased with HIV alone. The microenvironment in the lungs of TB patients may also be rich in cytokines, which stimulate HIV replication there.
  2. Hepatitis B has been implicated as a cofactor in two ways. Twu et al.. (1993) make a case for increased numbers of HIV seroconversions in individuals infected with active hepatitis B virus (HBV) after controlling for sexual behaviour and changes in disease over time. This suggests either that an existing active HBV infection is a cofactor which helps establish HIV infection after exposure, or that HBV is a ‘surrogate’ for other factors that perform that function. A second form of interaction is seen in increased disease severity in children infected with both HIV and hepatitis (Anitipa et al.. 1995).
  3. Another candidate cofactor is a member of the gamma lymphotropic herpes virus family, particularly HHV-8, which fulfils the ideal portrait of an HIV cofactor in Africa. Sero-epidemiological studies indicate a high prevalence of infection with HHV-8 in homosexual men in developed countries and a low prevalence in their general population, whereas in Africa there is a very high prevalence in the adult heterosexual population, particularly in East and Central Africa. HHV-8 strains are sexually transmitted in homosexual men in the West. However, in Africa, infection starts early in childhood and is probably achieved by other means of transmission, possibly because of poor hygiene. HIV and HHV-8 are mutual cofactors; HIV is a cofactor of the Kaposi Sarcoma induced by HHV-8. In Uganda the incidence of Kaposi Sarcoma among males, which was 14.6 per million during the period 1964–1968, increased by 1993 to 300 per million, representing 48.6% of all cancers diagnosed histologically and clinically at the Makerere University Hospital. This difference can be accounted for by the appearance of HIV in the interval between the two periods. The immuno-suppression induced by HIV favours the emergence of Kaposi Sarcoma tumour cells.

In turn, HHV-8 may be a cofactor of HIV transmission and AIDS progression. Monocytes are common targets of HHV-8 and macrophage tropic strains of HIV-1, allowing double infections. Moreover, it has already been shown that both HHV-8 and HIV-1 are present in semen.

The link between HIV and cofactors may explain why the epidemic in Africa is mainly heterosexual. This may be due to the concomitant presence of an epidemic of sexually transmitted disease in Africa as well as practices such as dry sex.

Control of AIDS will require the link between cofactors and HIV to be broken. The nature of the AIDS epidemic becomes a function not alone of prevalence, but rather a complex function of the interaction of HIV with cofactors.

II. Oxidative cofactors

It was reported to the panel that researchers from the USA and Malawi have shown that the deficiency of the anti-oxidant vitamin A is common among pregnant women in Africa, and that the deficiency is strongly associated with increased mother-to-child transmission of HIV.

2.4.2 Risk factors that are the primary cause of AIDS according to alternative hypotheses/theories

According to the alternative hypotheses/theories on the cause of AIDS that were presented in section 2.3 above, the following risk factors, and not HIV, are the primary causes of AIDS. The presence of HIV in AIDS patients can at best be that of a passenger virus that has no role in the cause or development of the disease.

Dr Giraldo made a presentation to outline the following risk factors that cause AIDS: Malnutrition

Malnutrition has been shown to result in:

  • Decreased tissue levels of reduced glutathione, one of the most important antioxidants that detoxifies reactive oxygen species and promotes cell growth.
  • Loss of weight, which according to some members of the panel may lead to the development of a positive HIV antibody test and not vice versa, as the HIV theory demands. In a study of Rwandan women over a period of 24 months, beginning in 1998, it was reported that nutritional status assessed by loss of body weight "was a significant predictor of eventual HIV seroconversion". Chemical stressors

Industrial chemicals and environmental pollutants are important causes of different abnormalities upon lymphocyte activation, proliferation and differentiation. Heavy metals, pesticides, diesel engine emission and food additives are also capable of this immune-suppression. Physical stressors

Exposure to lasers, electromagnetic fields, infrared light radio frequencies and free radicals have been shown to affect the immune system. Biological stressors

Human semen has been shown to induce chronic stimulation of the immune system with subsequent depression of the immune system. Blood and its components are known to be immuno-suppressive. Mental stressors

Different immunological abnormalities have been found in people under psychological stress. For example, anxiety and depression decrease lymphocyte counts. Bereavement decreases the response of lymphocyte proliferates to mitogen and lowers natural killer cell activity.

In concluding, Dr Giraldo proposed that at a physiological level, AIDS can be explained as a progressive degenerative alteration of different immune cells and immune metabolic reactions, secondary to multiple, repeated and chronic exposures to immunological stressors.

At a molecular level, AIDS is the result of alterations of immuno-competent cells and immune metabolic reactions due to an excess of free radicals, especially oxidising agents. Whilst the proponents of HIV as the cause of AIDS acknowledged that malnutrition and the stressors listed above will weaken immunity and increase vulnerability to HIV, these factors could not, on their own, result in the collapse of the immune system that is witnessed in AIDS patients. Nevertheless, Prof Montagnier requested that identification of the relative weights of these cofactors and/or risk factors on the immune system was vital to build up a rational policy on the prevention and treatment of AIDS.

2.5 Transmission of HIV and AIDS

Several of the panellists accept that HIV is blood-borne, transmitted through both heterosexual and male homosexual sex and vertically transmitted in breast milk from infected mothers to babies. However, as reported above, there were panellists who disputed that AIDS is an infectious and transmittable disease.

The latter panellists noted that HIV does not survive freeze drying yet haemophiliacs get AIDS. This was contested by Dr Williamson who noted that there are a large number of reports that have shown that transmission of HIV results in AIDS and a number of examples where it has been proven, by characterising the virus in both the donor and the recipient, that transmission has occurred. Furthermore, she stated that haemophiliacs who developed AIDS all received HIV contaminated blood whereas haemophiliacs who did not receive contaminated blood did not develop AIDS.

2.5.1 HIV Transmission as Estimated from ‘AIDS Deaths’

Some panellists disputed the estimated size of the ‘AIDS epidemic’ in South Africa.

Prof Duesberg pointed out that the figures for transmission of HIV in Africa as assessed by HIV seroprevalence do not tally with the WHO reported incidence of AIDS deaths over the past 15 years "which showed few AIDS deaths in 1985 rising to 50 000 annually in 1990 for the whole continent, reaching a plateau at 70 000 in 1992. For South Africa AIDS deaths in 1999 were estimated at 8 000." This suggested a rate of conversion from HIV to AIDS in Africa of 0.5% per annum compared to 3.5 to 5% per annum in the USA. He testified as to how mathematical models had consistently overestimated AIDS deaths; and the curious practice of the WHO of talking of cumulative AIDS cases and deaths rather than annual incidence. Even if the 75 000 cases reported annually by WHO for Africa are true AIDS deaths, this still represents only 0.6% of Africa’s annual mortality. He asked whether the scale of the epidemic had been determined by South Africans or by external agents.

The estimated mortality figures also did not tally with the growth rates in the population of 2.8% for South Africa and more for the rest of the continent, with Africa adding 150 million to its population in the first decade of the epidemic and 149 million during the second.

Dr Prozesky explained that because in South Africa AIDS is not a notifiable condition, there is a reluctance to record it as a cause of death on the death certificate, possibly resulting in an under-reporting of AIDS deaths. Furthermore, he explained, South Africans, not Americans, had described and quantified the scale of HIV seroprevalence through antenatal clinics. Dr Makgoba agreed with Prof Duesberg and Prof Mhlongo, that a National Register of AIDS deaths is needed.

Dr Fiala said that, "although all the predictions of the so-called AIDS experts of the mid-1980s for North America and Europe were totally wrong, this did not come as a surprise as these predictions were based on wrong data and assumptions". Dr Stewart believes that the predictions were wrong because lifestyle, rather than HIV positivity, determines the course of the epidemic. Dr Fiala noted that the diagnosis of AIDS in Africa is usually a clinical one, made by using the Bangui definition that is non-specific. (Note: Dr Makgoba had reported that South Africa used the US CDC definition of AIDS and not the Bangui definition). The usual infectious diseases in Africa could account for such deaths. He went on to illustrate the issues around the AIDS debate, thus:

  • Those suffering from well-known infectious diseases are diagnosed as suffering from AIDS.
  • Most scientific information about AIDS comes from Europe and the USA and developing countries are dependent upon it.
  • Through the AIDS discussion the industrialised countries have ensured themselves the right to determine the internal affairs of the developing countries such as budget distribution and assessment of health priorities.
  • In view of the shortage of resources it is not medically comprehensible why such funds should be spent on the documentation of HIV on the basis of unreliable tests and of AIDS on the basis of unsatisfactory definitions. Ultimately these funds are not then available for other areas.

Prof Mhlongo noted the inaccuracy in death certification in Africa, making estimates of AIDS deaths and therefore transmission difficult. Furthermore, he quoted Prof Coovadia’s textbook as attesting to poverty and poor socio-economic conditions as being the main causes of death in Africa. This includes malnutrition causing death from conditions such as Pneumocystis carinii pneumonia in neonates; dirty water causing diarrhoeal diseases; and overcrowding facilitating spread of infectious diseases.

Prof Montagnier pointed out that young adults in Africa were dying in great numbers and that Kaposi’s Sarcoma had risen from an incidence of 1% of cancers in Africa in 1980 to 40% in Uganda currently.

Dr Coll-Seck attested to the reliability of HIV seroprevalence testing in African countries, that she herself conducts, that indicated increasing transmission in these countries. Methods of surveillance used include special sentinel surveillance in antenatal clinics and anonymous linked special surveys. These are the basis of WHO’s figures.

Prof Duesberg asserted that in African studies of patients diagnosed clinically as having AIDS, 50% were later found to be antibody free suggesting the original diagnosis of AIDS was incorrect.

Dr Chalamira-Nkhoma reported that in Malawi the population growth rate from the census had been 3.2% in 1988 but only 1.9% in 1998, accompanied by a 10 to 20 fold increase in diseases such as TB. Other African panellists reported that deaths occurring in husbands followed by wives on a large scale in African villages were indicative of a lethal, STD (sexually transmitted disease) occurring.

Prof Geshekter quoted from two articles written by Morgan et al. that were published in Lancet in January 1998 and July 1997. As of 1987, there were approximately 1 to 1.5 million Ugandans said to be HIV-positive. However, according to the WHO's weekly epidemiological record of November 1999 the cumulative number of cases of AIDS reported in Uganda is 54,712. The question therefore is "what has happened to the other 946 000 HIV-positive Ugandans who after 10 years, evidently according to the WHO have not progressed to AIDS?"

2.5.2 Sexual Transmission

Dr Morris described a study published just a few months ago by Thomas Quinn showing that the level of virus in the plasma was directly related to the risk of transmitting to an uninfected person. Those individuals with undetectable levels of virus did not transmit to an uninfected partner. All the patients were antibody positive. The transmission data were true for both male to female transmission and female to male.

Prof Papadoupoulos-Eleopoulos quoted Dr Robert Gallo as saying in 1984 that ‘of 8 different sex acts, seropositivity correlated only with receptive anal intercourse’; and in 1986 that, ‘we found no evidence that other forms of sexual activity contributed to the risk’. She also quoted the Multicentre AIDS Cohort Study of 1986 as saying that it is the ‘frequency of passive anal intercourse and not the number of partners that is important’.

Others referred to Padian’s paper of 1997 in the American Journal of Epidemiology that showed that in a 10 year follow-up prospective study of heterosexual couples of whom only one partner of either sex was positive "no seroconversions occurred among exposed partners", suggesting no transmission via the vaginal route. They also noted Goudsmit’s view that for heterosexual HIV transmission anywhere in the world, including Haiti, Africa, and Thailand, ‘a homosexual or anal factor seems to be required’. The question was posed that if HIV is transmitted from active to passive partner in the sex act like other STDs, then how does the active partner become positive?

Dr Fiala noted that all the predictions of the scale of heterosexual transmission of HIV in Europe had not materialised, and new HIV infections had peaked in 1984 indicating that effect was not caused by preventive measures being taken. He had a sense of déjà vu coming to Africa and seeing all the dire predictions of pandemics, similar to those made in Europe and the USA in the late 1980s. He quoted from the 1997 Durex study of frequency of sexual intercourse that showed that Europe and the USA were world leaders in this regard while South Africa and Thailand lagged behind. Some panellists discounted market research done by Durex as questionable.

Prof Stewart reported that in 1983, when he took up leadership of the AIDS epidemiology work at WHO, "the speculation was that there would be a global pandemic spread by heterosexual sex of HIV. The fact was that with the data then available, or becoming available in the USA especially and also in Europe this was not so."

Dr Vella pointed out that in Italy, unlike other western countries, the initial cases of AIDS were spread by heterosexual contact, and consequently maternal-to-child remain the commonest mode of transmission in Italy.

Prof Abdool-Karim reported that there were data to suggest that the rapidly increasing seroprevalence for HIV in South Africa might be due to factors such as increasing pathogenicity of the several strains of subtype C entering South Africa; to cofactors such as STD; and to social dislocation caused by migrancy.

Prof Mhlongo pointed out that the data presented could be interpreted as suggesting that the HI virus is highly selective in terms of race. The high prevalence of HIV positivity in the black population of South Africa would therefore have to imply that black people were more promiscuous than white people. He went on to point out that there is no evidence to support such a conclusion. On the contrary, African people are very conservative in their sexual habits. The claim on the supposed promiscuity of Africans also contradicts the conclusions of the Durex study that Dr Fiala alluded to.

Dr Gayle presented evidence of sexual behaviour in youth in the USA with "38% of ninth graders already having sexual intercourse, and of twelfth graders 61%".

Dr Reddy highlighted the poor quality data on the psychosocial determinants of behaviour, on the environmental determinants of behaviour, and on the economic determinants of behaviour. She recommended questions in research be designed to look at and understand behaviour within the cultural context, and the ethnic context.

Dr Stewart revealed that, from his experience as an AIDS epidemiologist, predictions that were correct were those which were based on lifestyle and behavioural parameters. Thus drug addiction, men having sex with men and disadvantaged people, were good predictors of AIDS. But if seroprevalence was used as a guide to predict AIDS, one derived a gross over-estimate.

2.5.3 Mother-to-Child Transmission

For more than a decade, publications have addressed the possibility that HIV can be transmitted through breast-feeding. Several studies in Africa have shown that those HIV-negative infants born to HIV-positive mothers later tested positive when their mothers continued to breast-feed them. This was considered enough proof of the infectivity of breast milk.

Several panellists challenged these studies, questioning the rationale, which is based on an incorrect diagnosis. They argued that the researchers employed definitions in accordance with what is known or believed about HIV causing AIDS. HIV-1 infection was assessed by a positive PCR. HIV transmission was defined by a negative HIV-1 PCR at birth but a positive PCR one month later and was further confirmed by genetic relatedness between viral strains from the mother and from the child and viral strains from the breast milk. It was argued that both antibody and amplification tests for HIV can react positively to more than 70 other different conditions, all related to oxidative processes.

Dr Giraldo suggested that the only objective way to confirm the hypothesis of the transmission of HIV/AIDS through breast milk is by searching not only for HIV but also for all other potential risk factors for testing positively for HIV and immune deficiency in at least four different groups of people:

  1. One group of HIV-positive mothers and their infants living in a variety of African conditions
  2. One group of HIV-positive mothers and their infants living in a variety of developed conditions
  3. One group of HIV-negative mothers and their infants living in a variety of African conditions
  4. One group of HIV-negative mothers and their infants living in a variety of developed conditions.

In each group, there have to be a significant number of mothers that breast-fed exclusively, that used formula feed only and that mixed both forms of feeding. A retrospective questionnaire looking at past exposure, both voluntary and involuntary, to immunological stressor agents would need to be administered. Prospectively, all groups should be followed up for several years to establish if seroconversion to HIV-positive or the development of AIDS is secondary to exposure to immunological stressors.

Dr Morris reported that in the setting of mother-to-child transmission the viral load is a very predictive criterion for transmission of the virus to the infant. Women with undetectable viral loads or very low viral loads did not transmit the virus. It followed, therefore that by reducing the viral load in infected pregnant women with anti-retroviral drug therapies, one could prevent the transmission of HIV.

Dr Makgoba described a study based on data collected from the Perinatal Research Unit at the Chris Hani Baragwanath Hospital with a cohort of 504 infants of whom 54 acquired their HIV through mother-to-child transmission. After 18 months, 46 out of those 54 died. He also noted that mother-to-child transmission had been demonstrated by typing of viral nuclear material from mother and infant demonstrating that the same virus had infected both.

Further evidence for this mode of transmission was the fact that when certain anti-retroviral drugs were given to HIV-positive mothers during pregnancy transmission was significantly reduced.

Dr Rasnick quoted a paper by Coovadia et al. of follow-up of 133 infants born HIV-negative to HIV-positive mothers. Twenty-one of the cohort were exclusively formula-fed in the subsequent months, 36 were exclusively breast-fed and 76 received mixed feeding. Transmission rates among exclusively formula-fed infants were 24%, among mixed fed 32%, and 39% among breast-fed infants. How was it, he asked that some of the exclusively formula-fed, initially HIV-negative babies could contract the disease?

2.5.4 Blood-borne transmission and Occupational Exposure

In the report-back from the group of panellists who deliberated on prevention strategies, Dr Mossie reported that evidence for blood transmission had been derived from occupational exposure data, which the CDC had accumulated over time. From these data health workers who had been exposed through needle stick injuries involving their HIV-positive patients, had subsequently contracted HIV infection and sero-converted to HIV-positive status.

Studies conducted among drug users also proved that it was only when there was sharing of needles that HIV transmission occurred between them. The success of needle exchange programmes in reducing HIV transmission was also testimony to this fact.

Further evidence for blood-borne transmission has been derived from haemophiliacs who had contracted the virus from transfusion with infected blood products.

Dr Duesberg was, however not convinced by this evidence, expressing surprise that in Africa and also in the West very few doctors and healthcare workers had contracted this infection despite working with the so-called infected patients daily. He expressed concern that in South Africa, where such a serious epidemic was said to be occurring no data on hospital workers who had contracted HIV from their patients was available.

There was also another point of view expressed that healthcare workers appear to contract HIV but not AIDS. The focus of this argument rests on the contention, raised by Drs Rasnick and Bialy and Prof Duesberg, that despite having over 700 000 patients being treated for advanced HIV disease in the USA, no healthcare worker has been known to contract AIDS from exposure to HIV patients.

This was contradicted by the reported 17 reported cases of seroconversion in healthcare workers following needle-stick injury, with clear documentation of the patients’ sexual history included. Dr Bialy pointed out that this was very small incidence compared to that of healthcare workers contracting hepatitis following needle-stick injury. Others then rejoined that it is common knowledge that HIV is less contagious than hepatitis B, but it is still transmissible by blood and infected cells.

Drs Williamson and Gayle provided examples of healthcare workers who subsequently acquired AIDS from HIV transmission from accidental inoculation through contaminated instruments. The variability in the time it takes from HIV infection to AIDS was raised as a discrepancy regarding the transmissibility of AIDS.

The issue of viral latency as distinct from clinical latency as is the case with AIDS was raised. The early literature does not clearly indicate an increase in virus titre with progression of the disease. This was considered the hallmark of a passenger virus. However, a paper written by Fauci in Science showed clearly that the viral load was higher with progression of the disease. This notion was contested. Dr Morris presented data showing that the higher the viral load the greater the chance of developing AIDS within five years, the greater the chance of transmitting HIV to a sexual partner and the greater the chance of vertical transmission to babies.

Dr Turner requested clarification on the blood-borne transmission of HIV infection in haemophiliacs as the latter received plasma, which had been freeze-dried and stored prior to transfusion. Scientifically, the virus does not survive extreme conditions such as freezing and in the light of this fact how did freeze dried plasma still infect those who received it a few months after it had been stored. No explanation for this was proffered during the deliberations.

2.5.5 Epidemiology of Transmission

Prof Duesberg described the three classical hallmarks or the characteristics of an infectious epidemic that distinguish it from an epidemic caused by toxins or lack of nutrients.

  • Firstly the hallmark of an infectious epidemic, viral or bacterial, is that its increase in incidence is exponential. Incidence then declines within weeks or months as originally described by William Farr. The decline in incidence reflects spontaneous vaccination or immunity of the survivors. As a result microbial and viral infections are actually self limiting and typically seasonal; they degenerate over time producing a bell-shaped curve of incident cases.
  • Secondly the epidemiology of a microbial epidemic is typically random with no discrimination of heterosexuals from homosexuals; or men from women.
  • Thirdly the microbes that cause microbial or infectious epidemics are highly specific, reflecting the very limited genetic information of the causative viruses or microbes.

In contrast to this pattern, Prof Duesberg claimed, chemicals or toxins like nicotine, alcohol, cocaine or heroin; nuclear radiation; and lack of nutrients such as vitamin and protein deficiencies cause the epidemics. The kinetics or the time course of such epidemics are not specific because they are not self replicating. The dose and the duration of the toxin or the time of the lack of the essential nutrient determine the kinetics. They are not self limiting as there is no immunity against them – they are only limited by the withdrawal of the toxin or by the supplementation of the food with the missing nutrient.

The specificity of a non-infectious chemical or a drug-induced disease depends in part on the nature of the toxin and the nutrient that is lacking - it is typically not very high. An example would be the epidemic caused by smoking in America, or England. Smoking causes lung cancer, emphysema, heart disease, and bronchitis; but is not specific in the way a pneumococcus, influenza, hepatitis virus or a polio virus would be.

Prof Duesberg claimed that the so-called HIV epidemics in Europe and USA correlate exactly with the recreational drug epidemics followed by the ‘antiviral drug epidemics’. They started in America after the Vietnam War. Before then there were a couple of thousand heroin and cocaine addicts and there are currently in America 20 million daily users of illicit drugs, eight million of whom use hard drugs including cocaine, heroin, nitrate and amphetamines.

Quoting from WHO data, he showed that "the African AIDS epidemic is not exponential, it is not self-limiting and it is not bell shaped. It is unlike any microbial or viral epidemic that we have learned of so far. The kinetics are compatible with, let us say, a chemical epidemic like lung cancer and smoking or liver cirrhosis and alcohol or recreational drugs and AIDS in the United States or Europe".

The 1990 data from USAID he pointed out suggest that "there were 616 million Africans generating 75 000 AIDS patients, that is a very small percentage indeed. So, epidemiologically, this epidemic is restricted to a minority that appears to have in common malnutrition and poor sanitation. That is reflected by the clinical markers of African AIDS."

"So the epidemic appears to be non-randomly restricted to groups that are defined by malnutrition, poor sanitation and parasitic infection, as originally proposed by Anthony Fauci from the National Institute of Allergy and Infectious Diseases and Maurice Seligman from Paris who published in the New England Journal of Medicine in 1984 that African AIDS and AIDS in underdeveloped countries is due to parasites and malnutrition."

According to Prof Duesberg, the Bangui definition is explicitly unspecific. "Likewise, the anonymous AIDS notification forms from the South African Department of Health points out that weight loss over 10%, chronic diarrhoea for over a month, fever for more than a month, persistent cough, generalised periodic dermatatitis, recurrent herpes zoster, candidiasis, oral and oesophageal chronic persistent herpes, cryptococcal meningitis and Kaposi's Sarcoma, all of these are AIDS defining diseases. You could not get less specific than that. Thus the African AIDS epidemic is clinically complex and highly unspecific, unlike any microbial epidemic we have ever seen". Dr Makgoba pointed out that in South Africa the definition used for the diagnosis of AIDS was that of the US Centers for Disease Control and Prevention (CDC) and not the Bangui definition.

So in view of its clinical lack of definition and the lower than expected number of AIDS cases, the following question arises: Is the African epidemic new, like its US/European namesake, or does it comprise old diseases reported under a new name?

Dr Williamson recommended that "we need further studies in South Africa on the virus, to look at the natural history, the rate of disease progression in HIV infected people, is it shorter in Africa, is it shorter in South Africa and why is it shorter. Is this the effect of the cofactors that will result in increasing viral loads or are there other effects that we do not know about that are resulting in shorter disease progression? Although, in fact, there are no data to indicate that there is shorter disease progression in South Africa."

Dr Williamson also mentioned that the other unique feature in South Africa is the fact that we have a predominantly sub-type C epidemic in South Africa. Further basic research is needed on this sub-type to look at the unique properties of HIV sub-type C and see how this is impacting on transmission and pathogenesis.

For recommended research and studies please see Chapter 9.

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