Critics of the link between HIV and AIDS have raised the following key criticisms of the evidence:

• no animal model exists for AIDS; it is said to be impossible to inject an animal with HIV and cause AIDS
• viruses are said to cause disease quickly or never
• antibodies are usually protective, so why is it only HIV-positive people who develop AIDS?
• many cases of AIDS without HIV are claimed to exist, casting doubt on the role of HIV in the development of AIDS
• the failure of AIDS to spread outside the high risk groups is said to cast doubt on whether it is really an infectious disease
• HIV is claimed to be present in such low levels in the blood of people who are HIV- positive that it can't possibly cause disease. Furthermore, if it is so difficult to isolate, how come it's transmissible?
• the variance in the incubation period between infection with HIV and the development of AIDS is said to cast doubt on the link between HIV and AIDS
• the accuracy of tests for HIV is questioned

Animal models for HIV infection and AIDS

HIV belongs to a class of retroviruses called lentiviruses, or slow viruses, so called because they have been observed to cause disease slowly (Levy, 1993). The lentiviruses have a similar cellular and genetic structure, which is far more complex than other retroviruses. Three in particular have an almost identical structure immunodeficiency viruses affecting cats, monkeys and humans. In each species, infection with the virus causes a similar array of symptoms the loss of white blood cells bearing the CD4 marker, an illness just after infection and then a long period of CD4 cell loss before symptoms of severe immunodeficiency appear. In each species, antibodies against the virus are not protective.

Another curious feature of the immunodeficiency viruses which has given rise to misunderstandings is, by and large, their adaptation only to single species. Critics of the HIV-AIDS link have argued that because HIV does not cause illness in monkeys, it cannot cause AIDS in humans. However, there has been a report of a chimpanzee developing AIDS about 10 years after injection with HIV (Novembre, 1996), and it has also been demonstrated that baboons infected with HIV-2 developed an AIDS-like syndrome within two years of exposure (Barnett, 1994).

To establish that SIV is the true cause of an AIDS-like syndrome in monkeys, scientists have taken SIV and genetically engineered the virus to ensure that absolutely no other material from either the host animal or other infectious agents is bound up with the virus, and then injected it into monkeys to see whether it caused disease. These experiments showed that SIV alone, without any other agent, is capable of causing immune deficiency in a normally healthy monkey.

Each of the immune deficiency viruses has also been observed to cause CD4 cell loss in the body but not in laboratory culture, suggesting that these viruses interact with the host immune system to reduce CD4 cell numbers rather than killing CD4 cells directly.

Viruses cause disease quickly or never

This claim over-simplifies what appears to happen not only in HIV infection, but in many other infectious diseases. Many diseases are characterised by a relatively mild primary infection followed by much more severe illness later on. For instance, the primary infection seen in syphilis consists of a sore at the site of entry, followed by a rash and fever some weeks or months later. Left untreated, syphilis will subsequently develop into a much more serious disease in later years.

In all immunodeficiency virus infections, the primary infection features a fever and a period of enormous virus replication, followed by a very effective immune response which dramatically reduces the amount of HIV that can be detected in the bloodstream. Over a period of years the population of CD4 lymphocytes is reduced, although experiments with immunodeficiency viruses in other species suggest that a small proportion of individuals will suffer little immune system failure.

Why aren't antibodies against HIV protective?

HIV infection is by no means the only example of a disease in which antibodies fail to protect against the development of illness. Antibodies to herpes viruses such as simplex and varicella zoster do not prevent the re-emergence of these viruses from nerve tissue years after the initial infection. Primary poliovirus infection leads to a strong antibody response in every individual exposed, yet some individuals nevertheless develop paralysis.

AIDS-defining illnesses without HIV

Critics of the HIV-AIDS link say that they are particularly sceptical because of the thousands of the HIV-free AIDS cases now documented. In fact, this is one of the weakest parts of their argument.

Critics have tended to draw attention away from what is unusual about AIDS by arguing that the current AIDS definition is tautologous. Their objection is that people with opportunistic infections associated with immune suppression are only said to have AIDS if they are HIV- positive, meaning that by definition you can't be diagnosed with AIDS unless you have HIV. People with the same opportunistic infections who do not have HIV are not said to have AIDS. Thus, the link between HIV and AIDS is reinforced simply by virtue of the AIDS definitions (to their mind) unproven inference that HIV is the cause of the immune deficiency in people with AIDS. Professor Peter Duesberg has claimed that there are more than 5,000 cases of people with AIDS-defining illnesses who do not have HIV, allegedly making a nonsense of the suggestion that HIV causes AIDS.

Dr Steve Harris of the University of California has demonstrated the flaws in this argument. He points out that what is unusual and new about AIDS, and requires that we classify it as a new syndrome, is the development of immune deficiency as the result of the loss of CD4 lymphocytes in people who would not normally be expected to develop immune deficiency. Even if AIDS was to be redefined, omitting the need for HIV to be present but including the need for CD4 deficiency, most of the so-called HIV-free AIDS cases are still clearly different from genuine cases of AIDS and do not meet this new definition.

People who are at risk of non-HIV-related immune deficiency include the elderly, transplant recipients, the severely malnourished, sufferers from cancer, tuberculosis and other diseases known to have effects on immunity, or those exposed to radiation. But in each of these groups the precise nature of the immune deficiency, revealed in immunological tests, is different from that seen in AIDS. Only in the past fifteen years has a form of immune deficiency emerged which is characterised by a severe deficiency of CD4 lymphocytes as opposed to any other components of the immune system.

Dr Harris points out that even if HIV is left out of the equation, many of Duesbergs 5,000 cases of immune suppression can be clearly distinguished from AIDS because they do not match this distinctive pattern of life-threatening CD4 depletion. They are cases of mild or unexplained immune deficiency. For example, in 1992 several cases of immune deficiency without HIV were reported at the International AIDS Conference in Amsterdam. More such cases have come to light since; they are now known as idiopathic CD4+ T-lymphocytopenia, or ICL. Investigation has established that these cases have a number of common features which make them quite distinct from AIDS:

• They had no recognised risks for HIV infection, such as drug use or sex with people in high-risk groups
• As well as low CD4 counts, they often had low CD8 and total lymphocyte counts, a phenomenon not seen in classic' AIDS patients
• Their CD4 counts did not decline steadily, but went up and down dramatically over the years
• They often recovered spontaneously

Another explanation for 'AIDS without HIV' dates from the time prior to the development of viral testing, when antibody testing was the only way to determine whether someone had HIV or not. It has since been established that some people infected with HIV do not develop antibodies, due to immune dysfunction, so they appear to be uninfected (Ellenberger 1999).

Duesberg has also claimed that many HIV-negative people in the recognised high-risk groups (gay men, drug users and people living in Africa) also develop AIDS diseases. But close examination of his examples reveals that he has included many cases of people with signs of moderate immune deficiency who would not be diagnosed with AIDS even under the current definition. In fact, researchers have looked for cases of severe immune deficiency without HIV in the high risk groups and failed to find any such inexplicable cases. In all cases where control groups of HIV-negative men exist, the only people who have severe immune deficiency in the absence of HIV are those with other well-established immunosuppressive risks, such as radiation treatment for cancer.

Duesberg and other dissidents have argued that AIDS-defining illnesses were common in the high risk groups before they were identified as symptoms of acquired immune deficiency, or were misdiagnosed as other problems. Epidemiological evidence fails to support this view.

The reason that AIDS was identified as a distinct syndrome in the first place was because of the emergence of unusual illnesses in groups of people who had not hitherto manifested those illnesses. For example, prior to 1979 it was exceedingly rare for younger men to develop Kaposis sarcoma; by 1984 never-married men in San Francisco were 2,000 times more likely to develop Kaposis sarcoma than during the years 1973 to 1979 (Williams). Prior to June 1980 the Centers for Disease Control had registered only one request for pentamidine, the sole drug recognised for treatment of Pneumocystis carinii pneumonia (PCP). By December 31st 1994 127,626 cases of PCP in individuals with AIDS had been reported to the Centers for Disease Control.

Duesberg has also argued that the AIDS definition in Africa merely reclassifies people suffering from diseases such as tuberculosis, leishmaniasis, malaria and malnutrition which have been present for centuries into an artificial new category of AIDS. Whilst it is true that these conditions affect immunity, there is widespread agreement amongst doctors working in Africa that AIDS is a new syndrome which differs from the illness caused by the old' diseases long seen in Africa (Konotey-Ahulu). It is hard to understand how doctors would have come to decide that a new' syndrome was affecting Africa when they had considerable experience in recognising the symptoms of the `old' diseases Duesberg claims are being mistaken for AIDS. Indeed, the presence of a new disease in Africa was first signalled by a increase in cases of cryptococcal meningitis which was recognised as something new and unusual.

However, in the case of tuberculosis, it is possible that some people who are HIV-negative will be classified as suffering from AIDS in countries where HIV testing is not always possible, or where mycobacterial infection might be causing a cross-reaction on HIV antibody tests.

The failure of AIDS to spread outside the high risk groups

Just because HIV and AIDS have not spread outside the first groups in which they were identified, it does not necessarily follow that HIV should be dismissed as the cause of AIDS. Nevertheless many critics of the HIV-AIDS link have insisted that the ongoing failure of AIDS to appear outside the high risk groups adds strength to the argument that lifestyle factors rather than HIV are responsible for AIDS.

It is quite possible to explain the failure of AIDS to spread outside the high risk groups without having to dismiss HIV as the cause of AIDS.

HIV has been found in all the risk groups in which AIDS has appeared, but no other common factor is shared by all the risk groups, and no other factor has been shown to be associated with the distinctive depletion of CD4 lymphocytes in the same way. Some have argued that AIDS emerged in different risk groups at similar times because of different risk factors which deplete cellular immunity. According to this argument, it is a coincidence that HIV appeared at the same time in these different risk groups, and a coincidence that the presence or absence of HIV can be matched so closely with the development of AIDS in the different risk groups.

However, those who accept the association between HIV and AIDS point out that HIV has failed to spread widely amongst heterosexuals in the developed world due to a lack of pathways for the virus. Further discussion of the ways in which HIV has spread can be found in the AIDS Reference Manual.

Small quantities of HIV in the blood

Critics of the HIV-AIDS link have argued that HIV can only be isolated at very low levels in the blood of asymptomatic individuals too low for it to be causing the widespread immune damage it is said to cause.

This view is based on outdated research from a time when todays sophisticated tests for detecting and measuring the amount of HIV in the body were not available.

Critics of the HIV-AIDS link argue that increasing viral load is not the cause of immune suppression. They believe that the immune suppression is caused by other factors such as drug use, and that it is the loss of immunity that allows more HIV to grow (harmlessly) in the body. However, a number of studies have nevertheless shown that people who have high levels of HIV in their blood are at increased risk of a subsequent decline in CD4 cells and the subsequent development of AIDS. In other words, increasing viral load precedes the fall in CD4 lymphocyte levels and the development of symptoms of immune deficiency.

Is HIV transmissible?

Some critics of the HIV-AIDS link argue that HIV cannot be the cause of a transmissible condition, as the orthodox view maintains, since HIV levels in body fluids are too low for the fluids to be a source of infection.

Those who claim that HIV is not transmissible often cite the fact that in many cases, the sexual partners of HIV-positive individuals remain HIV-negative despite repeated unprotected sex. It is undoubtedly the case that in some risk groups the rate of transmission from one partner to another is low. This is probably due to the nature of their sexual practices: anal intercourse is a far more efficient transmitter of HIV than vaginal intercourse. But it has also been shown that the strain of HIV may play a major role in determining the chances of transmission. Sub-type E HIV is far more easily transmitted during vaginal intercourse than sub-type B HIV, which is the strain which is dominant in North America and Europe (Soto-Ramirez).

Also, the fact that infectivity appears to vary according to the stage of infection will also affect the likelihood of transmission. Viral load is very high during the early weeks of HIV infection, and by implication infectivity will be greatest when viral load is highest. This means that HIV would be expected to spread most rapidly in those populations which have the highest rates of partner change or needle sharing in the shortest period of time (Ho).

Variance in the incubation period

It is argued that the radically different times between infection with HIV and the onset of AIDS undermines the belief that HIV plays the key role in the development of AIDS.

This argument is often used to dismiss HIV as the cause of AIDS, based on the view that most illnesses have a standard incubation period. Yet syphilis exhibits similar variable incubation periods, with a primary illness followed by a long incubation period which can last years or decades and produce all manner of symptoms, severe in some individuals but almost imperceptible in others. This phenomenon has never been considered reason enough to reject Treponema pallidum as the cause of syphilis.

The cause of the variable incubation period has been located in the virus itself. HIV is not one single strain of virus, but many variants, and there are at least three substantially divergent strains (HIV-1, HIV-2 and type O) which exhibit substantially differing pathogenic effects. Whilst HIV-1 often causes disease rapidly, HIV-2 appears to take considerably longer.

Australian researchers have demonstrated that one reason for the differences in the asymptomatic period between HIV-positive individuals may be the characteristics of the specific strain of virus with which they are infected. Using New South Wales Blood Transfusion Service records between 1980 and 1985, the team identified 25 individuals with transfusion-acquired HIV infection for whom the exact dates of the infection in the eight donors who provided the infected blood could be established. Progression to AIDS and death was significantly slower in people who received blood from donors with slow disease progression than in those with blood from donors with faster progression. Median survival in recipients from donors who progressed to AIDS with five years was just over two years, but it was more than nine years for those who had received blood from donors who had still not progressed after 11 years (Ashton).

Age is the only clear co-factor to have emerged from cohort studies; older people are likely develop AIDS quicker. There may be a number of reasons for this. Firstly, immune competence declines with age. Secondly, it may be the case that during their lifetimes older people will have acquired a greater number of organisms which interact with HIV to make the virus replicate faster.