A.I.D.S., Africa, and heterosexuals

Press, 11 February 1986, Page 20

A.I.D.S., Africa, and heterosexuals

The second of two articles from “The Economist,” London, on the spread of the acquired immune deficiency syndrome. The first was printed on this page yesterday.

Most scientists believe that A.I.D.S. started in Africa and that it is a heterosexual disease there.

Although information is scanty (only Kenya officially admits to the World Health Organisation that it has A.I.D.S. cases) it appears A.I.D.S. is spreading east, south, and west from a source somehwere between eastern Zaire and western Uganda (where A.I.D.S. is known as “slim disease”). In this area as many as one in ten people may be infected. Elsewhere, the virus is mostly confined to the towns.

The most alarming information comes from Rwanda, where scientists from the St Pierre University Hospital in Brussels have been tracking the disease for two years. In the capital, Kigali, 18 per cent of hospital workers and 17.5 per cent of young adults have antibodies. One in ten Rwandan blood donors is infected.

The Belgian scientists are convinced that heterosexual sex is the chief means of A.I.D.S. transmission in Rwanda. The virus infects prostitutes, single men, promiscuous husbands and their wives, and the children of infected women. The scientists argue that Rwandan society, with its high age of first marriage (about 28 in men) and habit of sexual abstinence for two years after the birth of a child drives men to prostitutes. The Belgians found that four out of five A.I.D.S. patients had had regular contact with prostitutes and those people who went to more than 24 prostitutes a year had the highest risk of infection. If prostitutes infect their clients, the problem is indeed serious.

In Nairobi, tests indicate that the proportion of prostitutes infected has risen from one in eight in 1983 to more than two in three today. In other words, more than 6000 of the estimated 10,000 whores in the city may now have the A.I.D.S. virus.

However, other explanations are advanced for the Rwandan data. One is that gonorrhea and syphilis, common among A.I.D.S. carriers, speed transmission by causing lesions which bleed during sex.

Another is the re-use of hypodermic syringes. Many prostitutes in Africa inject themselves with penicillin. Many of their clients also inject themselves with penicillin. If prostitute and client share needles, that could

spread A.I.D.S. Poor people in Africa think that throwing away a needle after one use is wasteful. >

Two bits of evidence are cited against the needle theory. The correlation between self-injecting and A.I.D.S. infection is poorer than the correlation between the incidence of sexually transmitted disease or the number of sexual partners and A.I.D.S. And while A.I.D.S. in Rwanda is common among adults, it is rare among teenagers and children of school age. Yet it is when they first go to school that people have most injections. ‘ Still, needles are a worry. As the infection spreads, so does the chance that the previous person injected has the virus. Similarly with sex. As a disease becomes common, less promiscuity is needed to encounter it.

In 1980, the average San Francisco homosexual had 40 sexual partners a year. In 1984, he had ten, but his chances of meeting the virus were almost as great because the disease had spread from 24 per cent to 67 per cent of his potential partners.

Heterosexual transmission of A.I.D.S. is possible; that much is certain. But it remains unclear whether, in the absence of gonorrhea, needles, anal intercourse and extreme promiscuity, sex could sustain an epidemic’s growth. Suppose that A.I.D.S. carriers give the virus to one in 30 of their sexual partners (taking into account that some of the relationships last longer than others). Given these figures, an A.I.D.S. epidemic will spread among heterosexuals only if the average person has more than 30 sexual partners in his or her life. But are these suppositions realistic? Nobody can say. A more practical question is how these figures would be affected by changes in people’s sexual habits. Dr Douglas Feldman of New York University is assured by New York prostitutes that they all insist on the use of condoms nowadays. Condoms help to prevent transmission. That may help to stifle the epidemic.

Dr Feldman has also been asking questions in Rwanda. The answers are discouraging. Of the 33 Rwandese men and women he interviewed, most were aware of A.I.D.S. but only one-third of them were aware that sex was probably the main method of transmission.

Dr Feldman sees little point in

encouraginga return to stricter moral standards in countries like Rwanda. Not only has the problem gone too far — with nearly one adult in five in Kigali infected, people no longer have to be very promiscuous to encounter the virus — but banning prostitution would merely drive it underground. He wants a big campaign to encourge the use of condoms. Arguing where A.I.D.S. started may seem futile. It is not. If the disease started earlier in Africa, it must also have advanced further there. The African epidemic could, therefore, be a vision of America’s and Europe’s future. The case for suspecting that A.I.D.S. started in Africa is strong. The first cases in Europe were Africans, seeking medical treatment. About three-quarters of A.I.D.S. cases in Belgium are among Africans — though more than half were living in Europe when the symptoms appeared. The Belgian connection implicates Belgium’s former African colonies, including Zaire. and Rwanda. But it also helps to confirm that A.I.D.S. is a new disease in Africa, not some longstanding infection. Africans with A.I.D.S. have appeared in Belgian hospitals only since 1979.

This is confirmed by medical records from Africa. Kaposi’s sarcoma and cryptococcal meningitis, two disorders rare except among A.I.D.S. patients, have grown suddenly commoner in Kinshasa hospitals since 1978. Uganda, admittedly, is one of the places where Kaposi’s sarcoma has always been common, but the A.I.D.S. version is very different and did not appear at all in Zambia before 1983. Another way to trace the history of the disease is to reexamine old blood samples. Although this method is not entirely reliable, an apparently infected sample from (then) Upper Volta was taken in 1963, another from Zaire in 1970 and some from western Uganda in 1972-73. These results could mean either that A.I.D.S. was present but rare before 1978, or that it periodically invaded man from animals and later died out. New diseases arrive in one of two ways: from the transformation of a previously harmless version of an organism — (Dutch elm diease turned virulent after being in America), or by jumping from another species (myxomatosis jumped into European rabbits from a South American cousin). In the case of A.I.D.S. the first theory has been knocked on the head by the discovery that the virus is not, as was thought,

similar to human leukaemia viruses also common in Africa. It is instead of a kind (the lentiviruses) known only from animals.

If it did jump from another species, analogies like myxomatosis suggest it should be a closely related species — a monkey or ape. Dr Myron Essex of the Harvard School of Public Health found a similar virus in captive macaques, where it seemed to cause a similar disease. He then studied the commonest wild African monkey,' the green or vervet monkey, and found a similar virus in 40 per cent of those he looked at.

His assistant, Dr Phyllis Kanki, has shown the monkey virus to be genetically very similar but not identical to the A.I.D.S. virus. When blood samples from American A.I.D.S. patients are tested for the monkey virus, only about half cross-react; when samples from African victims of the disease are tested, nearly all cross-react.

One implication of this result is that many Africans whose blood reacts to the A.I.D.S. blood tests are infected with the possibly harmless monkey version of the virus (no green monkey has yet been seen to suffer from A.1.D.5.) and not the human one.

This is supported by a study in Senegal by Dr S. M’Boup and others at the Centre Des Maladies Sexuellement Transmissibles in Dakar, which found that 6.9 per cent of 289 prostitutes and 4.9 per cent of 122 surgery patients in Dakar had antibodies to the A.I.D.S. virus in their blood. Since Senegal has no A.1.D.5., these people probably have the monkey virus, not the human one.

Which leads Dr Essex to a wild surmise. If the monkey version is harmless, but causes an immune reaction which works against the human version, might not infection with the monkey version be tantamount to vaccination? X.

Copyright, “The Economist.”