Document:Stewart defends Adams

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The Lancet

Notes and News

AIDS and HIV: A Myth?

6 May 1989

In an age when bacteria were sought as the explanation for a host of man's afflictions, Koch's postulates provided a much-needed douche of cold water. They have not proved wholly successful for viruses, and there is no reason to suppose that retroviruses will be an exception to that relative failure. Furthermore AIDS is still a new disease, having been recognised only in the past decade, even though in retrospect earlier cases have come to light. It is wrong, then, to charge those who accept that HIV is the cause of AIDS with "moving the goalposts", as Jad Adams does in his spirited attack on received wisdom. His view that antibody equals protection – i.e. that HIV seropositivity in an individual who has AIDS suggests that the virus does not cause the disease – is also far too simple. Adams, who draws on Peter Duesberg's provocative article in Cancer Research in 1987, does an excellent job of summarising doubts about AIDS/HIV. He complains that in the late 1980s alternative theories are not getting a fair slice of scientists' attention. Many of the theories are rather eccentric, however, and the notion that there might be a co-factor (another virus, for example) has had quite an airing. So what hypotheses are they that are being brushed aside by the research funders? HIV does not cause AIDS, he says, offering vaguely "Another pathogen, perhaps so far identified and perhaps not", as the causative agent. Some treponema-like organism, if his chapter on syphilis is anything to go by. And where would that leave HIV?

Letter to the Editor

Uncertainties About AIDS and HIV

10 June 1989

SIR — The work of Prof. Peter Duesberg (1) and the questions posed by Jad Adams' book (2) merit more than a cursory note (May 6, p. 1031). Alternative hypotheses about the cause of AIDS are entirely appropriate in a setting in which the prevailing hypothesis has led, before validation, to the dogma that most people with antibody to HIV will proceed to AIDS (3, 4) and that a pandemic will ensue (5).

Duesberg's observation that HIV does not fulfill Koch's postulates can, arguably, be set aside on the grounds that many other pathogenic viruses do not meet the postulates either. But certain facts cannot be set aside. On average, HIV-1 remains latent for seven years or more before AIDS develops; the virus is not readily isolated; it multiplies slowly or not at all in vivo; and it has limited destructive power in infected cells (1, 6, 7).

In the policy forum convened by the American Association for the Advancement of Science, after the fifteen months of silence which greeted Duesberg's invited review on retroviruses, (1) Gallo's team (8) regarded the "Strongest evidence that HIV causes AIDS" as the development of "Features characteristic of a predictable sequence resulting in clinical AIDS" (i.e. evidence from prospective epidemiology). To those of us who hesitate to question the molecular biology, the epidemiological evidence is more easily understandable but no less questionable. Infection with HIV-1 seems to be followed mainly be a brief glandular fever, variable seroconversion, and prolonged latency before development of AIDS in a variable minority, so far, of seroconverters. The symptomatology is protean and there is a curious spectrum of morbidity which is partly host-specific (Kaposi in promiscuous male homosexuals); largely marasmic, as in many drug addicts without AIDS; partly microbial from a mass of other viruses, bacteria, fungi, protozoa, and opportunistic pathogens; and partly geographic, there being differences in transmission and pattern of disease in Africa, the USA, and Europe.

Outside Africa, AIDS develops almost exclusively in people with a narrow range of risk factors – namely, promiscuous male homosexuals practising penetrative intercourse, addicts who share needles, recipients of infected blood or blood products, prostitutes and their clients, and babies born to infected mothers. Many organisms besides HIV are transmitted thus and can exhaust immunity without the cytocidal assistance of HIV in a minority of infected T-lymphocytes and in some macrophages.

The main argument against HIV-1 as the unique cause of AIDS in all regions except, perhaps, Africa is the rarity of cases in persons without these risk factors who have been infected heterosexually or accidentally, or by routes other than penetrative sexual intercourse or needle-sharing. In the UK by April 30, 1989, the total number of people without risk factors presumed to be infected by heterosexual contact was only 8, out of 2,207 adult cases of AIDS (May 20, p. 1151) and only 17 cases in those who had partners with risk factors. There are few if any reports of AIDS in women exposed to infection from seropositive partners without risk factors. Even in the USA, with about 85,000 cases of AIDS and an unknown but much larger number of people (predominantly male) with latent HIV, the development of AIDS or AIDS-related complex in people infected heterosexually outside risk groups is still most unusual (9).

On these grounds, it could be argued that HIV-1 (and HIV-2) are behaving like other human retroviruses (HTLV-I and HTLV-II) which have specific properties and are prevalent in some parts of the world but almost always latent; and that AIDS coinciding with HIV-1 in certain communities is the end-point of complex but non-specific infectious, degenerative, and marasmic processes associated with risk-prone behaviour, exposure, or misfortune. This hypothesis is consistent with the observation that AIDS appeared primarily and spread explosively in localised male communities which began to engage in promiscuous homosexual intercourse and use of psychoactive drugs intravenously from about 1970 (10). The origin and spread of HIV-1, HIV-2, and of AIDS in Africa is something else.

Gordon T. Stewart


  1. Duesberg, Peter H., 1987. "[as Carcinogens and Pathogens: Expectations and Reality]" PubMed", Cancer Research, 1 March 1987, 47:1199-1220.
  2. Adams, Jad, 1989. AIDS: The HIV Myth, London: Macmillan.
  3. Moss A, Osmond D, Baccheti P, "The cause of AIDS", Science 1988; 242: 997.
  4. Liversidge, A, 1989. "AIDS" (interview with Robert Gallo), Spin 1989 (March); 54-56
  5. Gallo RC, 1986. "HTLV III: untangling the retroviral origin of the AIDS pandemic", Advances in Oncology, 1986; 2: 3-10
  6. Duesberg, Peter H., 1988. "[is not the cause of AIDS]" PubMed", Science, 241: 514-516.
  7. Duesberg, Peter H., 1989. "[immunodeficiency virus and acquired immunodeficiency syndrome: Correlation but not causation]" PubMed", Proceedings of the National Academy of Sciences, 86: 755-764.
  8. Blattner W, Gallo RC, Temin HM, 1988. "HIV causes AIDS" PubMed, Science 1988; 241: 514-517.
  9. Centers for Disease Control, AIDS Weekly Surveillance Report 1988 (August 8)
  10. Stewart GT, Gay GR, 1972. Trends in epidemiology, Springfield, Illinois: Thomas, 1972: chaps 9, 12