IS AIDS AFRICAN?

By Rosalind Harrison-Chirimuuta

Dissonance 22 May, 1997

From the beginnings of the AIDS epidemic in the early 1980's, western scientists have attributed its origin to black people, first in Haiti and then in Africa, yet the scientific literature that claims to prove an African origin is full of inconsistencies and sheer racist nonsense.

If human immunodeficiency virus (HIV) or some other as yet unidentified micro-organism is the cause of AIDS, there are a limited number of possibilities as to its origin: a human population that has harbored the virus for many years and from whom the virus has spread in recent years; an animal reservoir of the virus; or a mutation of an existing human or animal virus. The first possibility, a human reservoir for HIV, the "isolated tribe" or "village disease", was presented in detailed form in 1984, (1) but this hypothesis entirely disregards the historical record. For many centuries before the Portuguese sailed around the Cape, powerful west African kingdoms conducted trade across the Sahara to the Mediterranean, and every year many thousands of west Africans made the pilgrimage to Mecca. (2, 3) On the east African seaboard, city-states flourished on trade between central and southern African kingdoms such as Monamatapa in Zimbabwe, and Asia as far as Ming dynasty China. (4) With the advent of the Portuguese four hundred years of the African slave trade began. Millions of Africans were transported to the New World and Europe. African women were regularly raped from the time of capture. (5) Following the demise of the slave trade came the scramble for Africa, when almost the entire continent was colonised by the European powers. If AIDS was the cause of a tumour as common as Kaposi's sarcoma in equatorial Africa, the disease would have spread to the rest of the world hundreds if not thousands of years earlier.

Reading the scientific literature about a simian (monkey) origin for the human immunodeficiency virus can be a confusing business. It is easy to gain the impression that simian retroviruses can readily infect humans, but evidence for this is minimal. The simian immunodeficiency viruses (SIVs) that have been isolated from monkeys are, like all other retroviruses, species specific: in nature no monkey retrovirus normally infects a human or indeed a different species of monkey, and there is no monkey reservoir for HIV. (6) Only chimpanzees have been reported to be successfully infected with HIV, but they do not become ill. (7) A simian origin for HIV thus requires two chance events, a mutation of a monkey virus into a virus that could infect a human, and blood-to-blood contact between the monkey with the mutant virus and a human. Even in human populations, AIDS is not very efficiently transmitted via limited blood-to-blood contact, much less so than Hepatitis B, as evidenced by the minimal risk of becoming seropositive from needle stick injuries between medical personnel and patients. (8) AIDS researchers have claimed that Africans inject themselves with monkey blood or give their children dead monkeys as toys. (9, 10) Africans have rejected these claims as preposterous. (11) Even for the minority of Africans who hunt and eat monkeys, the prospects for human infection with even a mutant strain of SIV would be remote.

The improbability of transmitting a mutant retrovirus from monkeys to humans has not stopped AIDS scientists from making wild speculations. Claims that SIV was similar to a virus isolated from west African prostitutes were disproved when the SIV was found to be a laboratory contaminant. (12, 13, 14, 15) Undeterred, scientists have estimated that SIV mutated into HIV in the last few decades, their conclusions based on estimates of the rate of mutation of these viruses and their degree of genetic dissimilarity. (16) Even if such an improbable event did occur, given the existing colonial ties and trading links between Africa and Europe, the virus would have caused an epidemic in Europe at the same time as — or before — the epidemic in the United States. Yet all the documented evidence points to an epidemic beginning in America and from there spreading to Europe. (17, 18)

Three other arguments have been presented in support of an African AIDS hypothesis that are in fact peripheral to the origin of HIV. First, a number of cases of AIDS-like illnesses have been reported in Africans or people who have been to Africa that predated the AIDS epidemic in America. (19, 20) These can only be considered evidence for an African origin for AIDS if they were genuine cases of AIDS, and if such cases only occurred in Africa. In reality sporadic AIDS-like cases have been reported in the medical literature for many years but, with few exceptions, only those with an African connection have been highlighted. (21, 22, 23) Two of these cases were investigated further and were found to be spurious. The Danish surgeon who worked in Zaire and died in 1977 has been given a great deal of attention in medical and popular literature, but a sample of her blood that had been preserved was found to be HIV negative, although this has only been mentioned in private correspondence and not in the medical literature. (24) The other, a Manchester seaman who sailed to many continents including Africa and died in 1959 has been regarded as the first documented case of HIV infection. Samples of his tissue were preserved and were reported as containing HIV, but when further tests were carried out in a different laboratory the original findings were disputed. (25)

Second, much of the evidence for an African origin for HIV comes from blood tests that are unreliable [see the Dissonance piece "Horton hears the W.H.O." for the global politics of AIDS testing in Africa]. No blood test is perfect, and all tests give some percentage of false positive and negative results. Reports of HIV-positive tests in African blood taken decades before the AIDS epidemic in America and Europe are particularly suspect because of the age of the samples and possibilities for contamination. (26) In patients who have more than average amounts of circulating antibodies in response to other infections, the chances of a false positive are higher. This is undoubtedly the case for people continually exposed to malarial infection and other parasitic and infectious diseases. (27) Evidence dating back to the mid- 1980s shows that false positivity was a major problem in both stored serum samples and in samples taken during population studies for HIV in Africa, but it has largely been ignored. (28, 29) Claims that new tests can now be trusted are also untenable. Research published in 1994 found that antibodies to Mycobacterium antigens (antibodies produced by patients with tuberculosis and leprosy) give a positive test for HIV. (30)

Third, the sheer scale of the AIDS epidemic in Africa has been used as an argument for African origins. In this scenario, AIDS must have been in Africa longer than elsewhere for it to have affected so many people. On the grounds that the health services of most African countries cannot afford the diagnostic tests for AIDS, the World Health Organization has different criteria for defining AIDS in Africa, based on signs and symptoms only, from AIDS in the rest of the world [see "Horton hears the W.H.O." for more details, in particular, "The Human Cost" for the effects mis-diagnosis]. (31) This case definition includes patients who have prolonged cough, fever and weight loss, the classic presenting symptoms and signs of tuberculosis and other diseases common in the tropics. Both clinical criteria and diagnostic tests that fail to distinguish between HIV and treatable diseases common in Africa are used, separately or together, to estimate the extent of the HIV epidemic in Africa.

There are other reasons to dispute the scale of the African AIDS epidemic. In the West, progression from HIV infection to AIDS is reported to be from 5 to 7% annually. (32) This ratio is a function of the rate of progression from infection to manifest disease. If the huge number of reported seropositive Africans are seropositive for the same reasons as their counterparts in the West, then they should be developing AIDS and dying at a comparable rate and the continent should be witnessing a death rate far in excess of that which is occurring. Seropositive Africans do have a higher death rate than non-seropositive Africans, but this would be the case even if the majority of the seropositives were false positives suffering from chronic malaria, tuberculosis or other diseases. (33) A further difficulty with the African epidemic is the equal or near equal sex incidence of seropositivity found in population studies. It is claimed that this is due to the heterosexual transmission of HIV in Africa. (34, 35) Studies in the West have shown repeatedly that HIV positivity is far more likely to be transmitted from semen donor to semen recipient (whether the latter is male or female) than the reverse, and there is no reason why this should be different in Africa. (36, 37) If heterosexual intercourse is the major means of transmission of HIV in Africa, HIV seropositivity and AIDS should disproportionately affect women. An equal sex ratio implies not sexual transmission but the converse, non-sexual transmission, and one obvious explanation would be that the large majority of seropositives in Africa are false positives due to malaria, tuberculosis and other infections that affect men and women equally.

If the evidence for an African origin is contradictory or insubstantial, are there any credible alternatives? One possibility that has been given scant attention in the vast scientific literature about HIV and AIDS is an artificial origin of a mutant virus. This would seem rather surprising, as the risks of mutant viruses emerging from laboratories has been widely debated for many years. In the early 1970's several molecular biologists also expressed concern at the risks of molecular biology, and published a book Biohazards in Biological Research. (38) In February 1975, at Asilomar in California, an international conference of molecular biologists agreed a policy of self-regulation that included "appropriate safeguards, principally biological and physical barriers adequate to contain the newly created organisms, [should be] employed", and "certain experiments . . . ought not to be done with presently available containment facilities." In the following years the debate entered the body politic, and by 1976 the National Institutes of Health released guidelines for research on recombinant DNA molecules, and the following year the Federal Interagency Committee on Recombinant DNA Research issued an interim report on Suggested Elements for Legislation that was subsequently enacted by the US government. (39)

It was virtually impossible for any molecular biologist researching AIDS in the early 1980's to have been unaware of the debate about the risks of molecular biology and the subsequent legislation regulating their activities. Even before the AIDS epidemic, retroviruses were the subject of intense research activity because of their ability to turn RNA into DNA, and their possible role in causing cancer. Hundreds of thousands of African green monkeys and other species have been exported from Africa to research laboratories in Europe and America, where they have been subjected to experimental infections and their tissues used in cell culture. If HIV is a mutant monkey virus, it is surely more probable that it came from a laboratory than from monkey with naturally mutated virus biting man somewhere in "darkest Africa." That the latter hypothesis and not the former has been pursued suggests that factors other than science have been guiding the activities of AIDS researchers.

Within the scientific literature about AIDS and Africa all the racist themes can be found underpinning arguments for which scientific evidence is contradictory or absent:

• Africans are primitive peoples living in isolated tribes cut off from civilization, so they could have harbored diseases for centuries before they spread to the rest of the world.
• They are evolutionarily closer to monkeys, thus could more readily acquire monkey diseases, perhaps by having sexual relations with monkeys or at least involving them in their sexual practices.
• They are sexuality unrestrained, and a sexually transmitted disease would therefore spread more rapidly amongst them than any other people.
• Their intelligence is limited and they cannot understand the complexity of a disease such as AIDS, and their objections to being attributed with its source are harmful to themselves and do not need to be taken seriously.

AIDS science has at its heart a small number of assumptions and at first glance it may seem difficult to understand why there is so little debate or even diversity of opinion among the many scientists participating in this complex research activity. Part of the explanation for this lies with normal scientific practice. Each field of science, or at least mature science, has a core of theories, described by Lakotas as the 'hard core' of research programs, (40) or, in a somewhat different conceptual framework, by Kuhn as paradigms. (41) Scientists working in the field are unlikely to challenge the existing paradigm, in part because of training and discipline, which can constitute a form of internal censorship, and in part from external peer pressure. The latter can be of a very practical nature, as scientific careers can only progress if funds can be obtained for research projects and the results of research are published in learned journals. Leading scientists in the field normally have influence over both the allocation of funds within their field of research, and, by the process of peer review and editorial control, publication in scientific journals.

Yet even 'normal' science does not function independently of its social, economic and political context. The days of the independent scientist conducting experiments in the study at home are long gone, and the political and economic priorities of government and industry now largely determine the allocation of funds. And, as scientists bring their own particular cultural baggage into their work , so too the results of their work are expected to conform with the prevailing cultural norms or vested interests. The manner in which science in the late twentieth century is organized and funded makes it possible for a small group of scientists very well connected to the political, military and industrial establishments to dominate their area of research, and in so doing, promote the interests of their sponsors even at the expense of scientific truth. *

References

1. De Cock KM. AIDS: An old disease from Africa? British Medical Journal, August 4, 1984, Vol 289 p306-8.
2. Davidson B. Old Africa rediscovered. Victor Gollancz Ltd, London 1959.
3. Robinson CH. Hausaland or fifteen hundred miles through Central Soudan. Sampson Low, Marston and Company Ltd, London 1900.
4. Garlake PS. Great Zimbabwe. Thames and Hudson, 1973.
5. Davidson B. The African Slave Trade. Little, Brown and Company, Boston/Toronto 1980.
6. Fukawawa M, Miura T, Hasegawa A, Morikawa S, Tsujimoto H, Keizaburo M, Kitamura T, Hayami M. Sequence of simian immunodeficiency virus from African green monkey, a new member of the HIV/SIV
7. Gajduser DC, Amyx HL, Gibbs CJ, Asher DM, Yanagihara RT, Rodgers-Johnson P, Brown PW et al. Transmission experiments with human T-lymphotropic retroviruses and human AIDS tissue. The Lancet June 23, 1984, p1415-6.
8. Jones P, Hamilton P. HTLV-III antibodies in haematology staff. The Lancet January 26, 1985 p217.
9. Noireau F. HIV transmission from monkey to man. The Lancet, June 27, 1987, p1498-9.
10. Green J, Miller D. AIDS The story of a disease. Grafton Books, London 1986, p66.
11. HIV origin 'a continuing mystery:' Green monkey theory disputed. Skin and Allergy News January 1988 Vol 19 No 1, p28-29.
12. Kornfield H, Reidel N, Viglianti GA, Hirsch V, Mullins J. Cloning of HTLV-4 and its relation to simian and human immunodeficiency viruses. Nature Vol 326 9 April 1987 p610.
13. Mulder C. A case of mistaken non-identity. Nature Vol 331 18 February 1988 p562.
14. Mulder C. Human AIDS virus not from monkeys. Nature Vol 333 2 June 1988 p396.
15. Connor S. Laboratory mix-up solves AIDS mystery. New Scientist 25 February 1988 p32.
16. McClure M. Where did the AIDS virus come from? New Scientist 30 June 1990 p54-57
17. Osborn JE. The AIDS epidemic: Multidisciplinary trouble. New England Journal of Medicine, Vol 314 No 12, 1986 p779-82.
18. Melbye M, Biggar RJ, Ebbesen P, Sarngadharan MG, Wiess SH, Gallo RC, Blattner WA. Seroepidemiology of HTLV-III antibody in Danish homosexual men: prevalence, transmission, and disease outcome. British Medical Journal Vol 289, 8 September 1984. p573.
19. Bygbjerg IC. AIDS in a Danish surgeon (Zaire, 1976). The Lancet April 23, 1983, p925
20. Corbitt G, Bailey AS, Williams G. HIV infection in Manchester, 1959. The Lancet Vol 336 p51.
21. Katner HP, Pankey GA. Evidence for a Euro-American origin of Human Immunodeficiency Virus (HIV). Journal of the National Medical Association Vol 79, No 10, 1987, pp1068-72.
22. Sterry W, Marmor M, Konrads A, Steigleder GK. Kaposi's sarcoma, aplastic pancytopaenia, and multiple infections in a homosexual (Cologne, 1976). The Lancet April 23, 1983, p924.
23. Williams G, Stretton TB, Leonard JC. Cytomegalic inclusion disease and Pneumocystis carinni infection in an adult. Lancet 1960; ii: 951-55.
24. Letter from Dr Bygbjerg to Dr Grote, April 18, 1988.
25. Researchers in US dispute first case of AIDS. British Medical Joournal Vol 310, 15 April 1995 p957.
26. Nahmias AJ, Weiss J, Yao X, Kanki P, Essex M et al. Evidence for human infection with an HTLV III/LAV-like virus in Central Africa, 1959. The Lancet May 31, 1986, p1279-80.
27. Biggar RJ. Possible non-specific associations between malaria and HTLV-III/LAV. New England Journal of Medicine August 14, 1986, Vol315 No 7 p457-8.
28. Hunsmann G, Schneider J, Wendler I, Fleming AF. HTLV positivity in Africans. The Lancet, October 26, 1985, p952-3.
29. Wendler I, Schneider J, Gras B, Fleming AF, Hunsmann G, Schmitz H. Seroepidemiology of human immunodeficiency virus in Africa. British Medical journal, September 27, 1986, Vol 293 p782-5.
30. Kashala O, Marlink R, Ilunga M, Diese M, Gormus B, Xu K, Mukeba P, Kasongo K, Essex M. Infection with Human Immunodeficiency Virus Type 1 (HIV-1) and Human T Cell Lymphotrophic Viruses among leprosy patients and contacts: Correlation between HIV-1 cross-reactivity and antibodies to lipoarabinomannan. Journal of Infectious Diseases 1994; 169: 296-304.
31. Weekly Epidemiological Record No 10, March 7, 1986, p71.
32. Anderson RM, May RM. Epidemiological parameters of HIV transmission. Nature Vol 333 9 June 1988, p514-522.
33. Mulder DW, Nunn AJ, Kamali A, Nakiyingi J, Wagner HU, Kengeya-Kayondo JF. Two-year HIV-1- associated mortality in a Ugandan rural population. Lancet 343 (23 April 1994): p1021-3.
34. Biggar RJ, Melbye M, Kestens L et al. Seroepidemiology of HTLV-III in a remote population of eastern Zaire. British Medical Journal Vol 290, 16 March 1985, p808-810.
35. Anderson RM, May RM, Boily MC, Carnett GP, Rowley JT. The spread of HIV-1 in Africa: sexual contact patterns and the predicted demographic impact of AIDS. Nature Vol 352, 15 August 1991, p581-589.
36. Heyward WL, Curran JW. The epidemiology of AIDS in the U.S. Scientific American. October 1988 p52-59.
37. Acheson ED. AIDS: A challenge for the public health. The Lancet. March 22, 1986, p662-665.
38. Hellman A, Oxman MN, Pollack R (eds). Biohazards in biological research. (Cold Spring Harbour, N.Y.: Cold Spring Harbour Laboratory, 1973)
39. Grobstein C. A double image of the double helix. The recombinant-DNA debate. WH Freeman and Company, San Francisco, 1979.
40. Lakatos I. The methodology of scientific research programmes. Cambridge University Press, 1978.
41. Kuhn TS. The structure if scientific revolutions. The University of Chigago Press, 1970.