recombinants, creating immense genetic heterogeneity, especially in the western equatorial region where the epidemic is oldest and the diversity of subgroups is greatest. Certain recombinant forms, however, have been especially successful. By 2005, 16 had been classified as circulating recombinant forms (CRFs), for each of which at least three distinct specimens had been analysed. The most successful were CRF01_AE, the dominant form of HIV in South-East Asia, and CRF02_AG, responsible for at least two-thirds of West African HIV infections.19 Recombination is probably at least as important as mutation in accelerating the evolution of HIV, but its implications for dating based on a molecular clock are complex and obscure. By blurring differences between subgroups it might make evolutionary events seem more recent than they really were, but by multiplying the number of strains it might make the events seem more ancient than they were. The two teams who estimated dates for the differentiation of the M group tried to exclude the effects of recombination, but geneticists feared that the problem was more difficult and that conclusions based on a molecular clock ‘may be of very limited value’.20
However uncertain their findings, attempts to date the epidemic clarified several problems in its history. Together with the identification of the 1959 case in Kinshasa, they effectively ruled out the theory, propounded in Edward Hooper’s fascinating book, The River, that the HIV-1 epidemic had been caused by a polio immunisation campaign in the Congo region during 1957–60 that allegedly used a vaccine bred on SIV-infected chimpanzee kidneys – a theory also contradicted by negative tests on surviving vaccine samples.21 Instead, attempts at dating stimulated interest in the interwar period when the diversification of group M supposedly began. Noting that the earliest known HIV cases in Africa all occurred in francophone territories, researchers highlighted colonial innovations there that might have converted occasional viral transmissions into a disease capable of epidemic expansion: penetration of the forest for hunting, rubber collection, and logging; increased viral transmission through labour concentrations and vaccine campaigns against sleeping sickness and smallpox; and the adaptation of the virus to humans through rapid passaging by arm-to-arm inoculation that would have the effect of accelerating evolution.22 No direct evidence linking these innovations 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.
