The African AIDS Epidemic. John Iliffe

to HIV had been published by 2005, but the problem of how a simian virus might become capable of causing a human epidemic attracted the attention of other researchers. HIV-1 group N and at least six transmissions of HIV-2 had not become sufficiently transmissable or infectious as to cause epidemics. These were the forms of HIV most similar to SIV, so it appeared that the mere transmission of SIV to humans was unlikely to cause widespread disease; the virus must have evolved from SIV to HIV within human bodies, and it must have done so for the first time and perhaps more or less simultaneously in two groups of HIV-1 and two of HIV-2. Preston Marx and others argued that the chance of this happening naturally was ‘vanishingly small’. Instead, rejecting the 1931 date for the diversification of the M group but accepting 1959 as the first documented HIV case, they suggested that SIV had been converted into HIV by rapid passaging through African populations during the 1950s, owing to the introduction of supposedly disposable (but often in practice re-used) syringes to inject penicillin and other new medications. Between 1952 and 1960 annual world output of syringes increased from 8 million to something approaching 1,000 million.²³

      These theories remained theories, but they indicated the kinds of evolutionary stages that may have produced HIV: probably multiple transmissions of SIV from sooty mangabey monkeys in West Africa over a long period; perhaps less frequent transmissions of the rarer chimpanzee virus in western equatorial Africa; its evolution into HIV within human bodies, whether over some centuries or through the unintended effects of medical interventions; and its emergence by 1959 as a virus capable of causing a global human epidemic.

      Yet a difficulty remained: there was no visible epidemic in 1959, nor for another twenty years. The likely reasons lay in three characteristics of the virus. First, as viruses go, HIV is difficult to transmit. Whereas influenza – ‘the sickness of the air’, as it was called in Ethiopia in 1918 – can be transmitted aerially to anyone close enough to inhale it, HIV can be contracted only by absorption of blood, genital fluids, or milk from an infected human body. In heterosexual intercourse – the chief means of transmission in Africa – the chance of infection in one sexual act between otherwise healthy partners has been variously estimated at between 1 in 10,000 and 1 in 500.²⁴ To create and sustain an epidemic, therefore, requires special circumstances, but the chance of transmission increases substantially if either partner has a sexually transmitted disease or if the already-infected partner is in a particularly infectious condition. This is the case shortly after infection, when a person is perhaps eight or ten times more infectious than usual, and in the last stages of the disease, when infectivity is even greater.²⁵

      The difficulty of transmitting HIV relates to the second likely reason for the slow emergence of a visible epidemic, which was the very gradual development of the disease within human bodies. For a few weeks after infection the virus has the advantage of surprise: viral load rises rapidly, lasting damage may be done to the immune system, and there may be feverish symptoms, perhaps often mistaken for malaria. Thereafter the immune system counter-attacks and an evenly matched war of attrition takes place in which HIV produces up to 10 billion new viral particles and destroys up to 2 billion CD4 helper T-cells each day. In HIV-1 this incubation period varies considerably but may last in adults for an average of nine or ten years – the period measured by a careful study in Uganda – before the immune system is so weakened that Aids supervenes. Death in untreated patients then follows almost invariably and relatively quickly, in an average of perhaps nine or ten months.²⁶ The infected person remains infectious throughout the disease. This long incubation period with only sporadic symptoms distinguishes HIV/Aids from previous epidemic diseases, renders it especially dangerous to human life, makes it difficult to check, ensures that it does not burn itself out, and, as will be seen, has given the Aids epidemic its unique character. As a comparison, the incubation period of influenza is not nine years but one to three days, while that of plague in Britain, considered unusually long and therefore dangerous, may have averaged about 30 days.²⁷ ‘What is serious,’ a West African villager said of HIV, ‘is that this disease is silent, hypocritical, visible only when the damage is already irreparable.’²⁸

      There was a third reason why the potentially epidemic virus that existed in 1959 did not breed a visible epidemic for another twenty years. HIV/Aids does not kill but destroys the immune system’s capacity to resist other opportunistic infections that are ultimately fatal. Some of these, notably tuberculosis, were infections already current in the region concerned, so that it may not have been easy to discern that a new disease was present. Retrospectively, however, these opportunistic infections are the signs that first reveal the emerging HIV epidemic. Their appearance in western equatorial Africa during the 1970s is the third reason – alongside the location of the simian ancestor and maximum diversity of subgroups – to believe that the HIV epidemic originated there.

      3

       Epidemic in Western Equatorial Africa

      HIV-1 first became epidemic during the 1970s in western equatorial Africa, its place of origin. It was at first a silent epidemic, unnoticed until established too firmly to be stopped. In this region, also, during the mid 1980s, the epidemiology of heterosexual HIV/Aids was first determined, exposing a pattern whose main features were to extend throughout sub-Saharan Africa but whose local peculiarities were also to limit epidemic growth within the western equatorial region itself. From this region, moreover, variants of the virus were carried to the rest of the continent.

      Although HIV-1 had almost certainly existed in western equatorial Africa since at least the 1950s, it had hitherto struggled even to survive in a sparsely populated region of difficult, often forested environments and poor communications. This was clear from a group of villages at Yambuku in the north of the DR Congo. Blood taken from 659 villagers there in 1976, during one of the first outbreaks of Ebola virus, later revealed that five (0.8 per cent) were infected with HIV. When the villagers were tested again ten years later, HIV prevalence was still 0.8 per cent. Of blood samples collected across the border in southern Sudan in 1976, 0.9 per cent subsequently revealed HIV.¹ Such low levels of infection may well have existed in other rural areas of the equatorial region during the 1970s. They apparently existed also in Kinshasa. One of those testing positive at Yambuku had probably contracted the disease in the capital during the early 1970s. Of 805 blood specimens taken from pregnant women in Kinshasa in 1970, two later revealed HIV infection. So did blood taken there in 1972 from two of four patients with Kaposi’s sarcoma.²

      The conversion of this low-level infection into an expansive epidemic probably took place in the urban environment of Kinshasa during the 1970s. The key may well have been the exceptional infectivity of the newly infected, which meant that if the virus entered a network of sexual relationships in which partners were exchanged rapidly and extensively, it could build up a momentum of infection sufficient to reach epidemic levels. That is probably what happened in the United States, where HIV prevalence among homosexual men attending a sexually transmitted disease clinic in San Francisco rose between 1978 and 1984 from 1 per cent to 65 per cent.³ It happened at much the same period, although less explosively, among heterosexuals in the East African cities of Bujumbura, Kigali, and Nairobi, as also in rural south-western Uganda and in Abidjan in West Africa. The first occasion, however, was in Kinshasa, where HIV first encountered rapid partner exchange in urban sexual networks wider, although not necessarily much more promiscuous, than those of the countryside.

      Map 1 Western Equatorial Africa

      The first person to notice the change may well have been Dr Kapita Bila, the Congolese physician heading the internal medicine department at Kinshasa’s huge, 2,000-bed Mama Yemo Hospital. ‘Something dramatic happened in 1975,’ he recalled a decade later, referring especially to a doubling of cases of Kaposi’s sarcoma, a tumour that could take aggressive forms when the immune system was damaged and hence often became a conspicuous symptom of Aids. Other hospitals in the region observed this increase only in the later 1970s and early 1980s, but Kapita Bila dated it at Mama Yemo from 1975 and claimed that hospital records revealed cases at that time. The records also confirmed Congolese doctors’ recollections that in the mid 1970s they