to epidemic proportions, but not the explosive proportion seen in Kigali. This was reinforced by the fact that over 90 per cent of men in the western equatorial region were circumcised, which probably provided some protection because the foreskin was especially liable to viral penetration, and that sexually transmitted diseases – although closely associated with HIV infection – were relatively rare, including the incurable genital ulcer disease caused by herpes simplex virus 2 (HSV-2) that was spreading throughout the world in synergy with HIV. A later comparison was to show that, thanks chiefly to these two advantages, Yaounde had significantly lower HIV prevalence than Kisumu in Kenya or Ndola in Zambia, despite high levels of extra-marital sex.34
These constraints help to explain the most remarkable feature of the HIV epidemic in western equatorial Africa: its failure to expand during the 1990s beyond the levels of prevalence reached early in the decade, although those levels were often at or above the threshold 3–5 per cent prevalence commonly thought to trigger exponential growth. In Brazzaville city, for example, prevalence at antenatal clinics fell between 1991 and 1996 from 8 to 5 per cent, suggesting, together with a peak prevalence in older age groups (men of 35–49 and women of 25–30), that this early epidemic had reached maturity at a modest prevalence.35 The epidemic in Bangui, similarly, stabilised between 1993 and 1998, although at a level of 16 per cent that could be sustained only by a high incidence of new cases.36 In Gabon and Cameroun, where the epidemic had begun later, there was more growth during the 1990s, but to adult levels below 7 per cent.37 The most striking illustration was the DR Congo, often considered ‘a risk environment par excellence’,38 where, however, the long-predicted epidemic explosion did not happen. In Kinshasa, for example, HIV prevalence among pregnant women declined between 1985–8 and 1992 from 6–7 per cent to 5 per cent and then remained at or below that level for the remainder of the decade.39
Analysts struggled to explain this surprising stability. Some suggested that the HIV strains evolved so early in this region might be less virulent than those elsewhere, but there was no hard evidence to support this. Others thought that poverty might have reduced the rate of sexual partner exchange.40 More convincingly, it was pointed out that in Kinshasa, as in Bangui, the epidemic, having begun so early, had reached a stage of maturity at which a stable prevalence concealed a balance between deaths among older groups and a substantial incidence of new infections, chiefly among the young. Between 1986–7 and 1989–90 in Kinshasa, for example, prevalence among pregnant women under 25 nearly doubled, while among older women it fell slightly. The investigators estimated that the annual incidence of new infections in pregnant women aged 20–24 was almost 2 per cent, nearly twice that in the general population. ‘A stable HIV seroprevalence in sentinel surveys,’ they concluded, ‘may be consistent with a dynamic epidemic.’ The city’s sex workers may have had a parallel experience, prevalence stabilising at about 35 per cent while annual incidence was 10 per cent.41
Both Kinshasa and the rest of DR Congo also enjoyed some protection against an explosive epidemic from the great distances between population concentrations and the difficulty of travel where transport had widely broken down and much violence and insecurity prevailed, these factors together preventing the linking of sexual networks that commonly fostered epidemics. The falsity of the common belief that ‘war creates the perfect conditions for the spread of AIDS’42 was also demonstrated at this time in neighbouring Angola, where national antenatal prevalence after nearly 40 years of warfare was found by a survey in 2004 to be only 2.8 per cent, with the lowest figures in central provinces ‘that have been more protected by the effect of war,’ as the Vice-Minister of Health put it.43 By contrast, the two countries registering modest epidemic growth during the 1990s, Gabon and Cameroun, were the most peaceful in the region.
The limited capacity for expansion shown by the western equatorial epidemic during the 1990s had as its counterpart the survival there – perhaps especially in the countryside – of a diversity of HIV subtypes and recombinant forms far greater than anywhere else in the world. A more explosive epidemic might well have swamped this diversity by a single dominant strain more like those created by founder effects elsewhere. Yet it was from this region that the various forms of the virus were carried to the rest of the continent and the world. The most spectacular illustration was the transmission of the circulating recombinant form CRF01_AE from its hearth in the northern DR Congo and the neighbouring Central African Republic, where alone it was common early in the epidemic, to become the major strain of HIV in South-East Asia, although the means of this transmission are unknown.44 A less dramatic example was the other major circulating recombinant, CRF02_AG, which provided 60 per cent of HIV-1 strains in Cameroun during the 1990s, especially in the north, and some 54 per cent in Gabon. Its ancestors probably lay in the DR Congo – one of them was a virus collected at Yambuku in 1976 – but CRF02_AG itself was rare in both Congos during the 1990s and appears therefore to have taken shape in the Cameroun-Gabon region, whence it was carried northwards to become the dominant form of the virus throughout West Africa.45 By contrast, the subtypes (as distinct from CRFs) of HIV-1 transmitted to other parts of the continent appear to have been carried directly from the DR Congo. Subtype A was the most common form there, especially in the north, and was carried into East Africa, where it shared predominance with subtype D, itself rare elsewhere except in the DR Congo.46 Less certainly, subtype C, which came to dominate southern Africa (and Ethiopia), was common only in the south of the DR Congo, whence it may have been carried southwards.47 The history of this radiation from the equatorial region is the next issue to consider.
4
The Drive to the East
Eastern Africa was probably the first region to which HIV was carried from its western equatorial origin, along several different routes that cannot now be traced in detail. The virus entered a region divided historically into two contrasting natural and social environments: the well-watered, densely peopled kingdoms around Lake Victoria and on the Ethiopian plateau, and the less centralised societies in the drier savanna country where population clustered only on highland outcrops, in colonial cities along transport routes, and on the Indian Ocean coast. This framework gave HIV/Aids in eastern Africa its distinctive contrast between explosive epidemics in the Lake Victoria basin and the capital cities, on the one hand, and slow penetration into the remainder of the region, on the other. Varying relationships between cities and countryside were especially important in the process, as were the mobile groups linking them together and the factors – widespread labour migration, male predominance in urban populations, low status of women, lack of circumcision, and prevalence of sexually transmitted diseases – that bred higher levels of infection than in western equatorial Africa.
The virus first entered the Lake Victoria basin bordering the DR Congo. Patients from Rwanda and Burundi were seen alongside Congolese in European hospitals during the late 1970s and early 1980s. They not only led expatriate researchers to visit Kigali as well as Kinshasa in 1983 but encouraged observers of the epidemic to believe that Rwanda, Burundi, and perhaps even Uganda had been simultaneous or even earlier places of origin alongside western equatorial Africa. The location of the chimpanzee host makes this unlikely, however, as does the distribution of HIV-1 subtypes, for there is no indication in the Lake Victoria basin of the diversity of strains found in the DR Congo. Until well into the epidemic, the A and D subtypes dominated the region.1
In Rwanda the first probable case recorded was a mother who displayed characteristic opportunistic infections in 1977 and subsequently tested positive for HIV along with her husband and three children.2 A retrospective study found that by 1982 some 12 per cent of blood donors in Kigali were infected. The team visiting the hospital there a year later identified symptoms of Aids in 26 patients.3 The virus had apparently established itself during the 1970s and reached epidemic proportions by the early 1980s. The evidence from Burundi is even stronger, for 658 blood specimens taken during a study of haemorrhagic fever there in 1980–1 later revealed an HIV prevalence of 4.4 per cent, reaching 7.6 per cent in Bujumbura and 2.8 per cent in the countryside, at a time
