pregnant women were infected in 1988–92, with one area of high prevalence (14 per cent) at Katima Mulilo in the Caprivi Strip, which was not only the headquarters of the South African army but a meeting point of long-distance transport routes from Angola, Zambia, Zimbabwe, Botswana, and Namibia, notorious for high levels of commercial sex. Once Namibia was assured independence in 1990, however, some 43,387 registered exiles returned, mostly from Angola and Zambia. Many may well have been infected, for in 1992–3 prevalence was 17.2 per cent among Namibian soldiers in the northern Ovamboland region, many of them previously based outside the country. During the mid 1990s Namibia suffered an explosive epidemic, antenatal prevalence rising from 4 per cent in 1992 to 21 per cent in 2001. The northern nuclei at Katima Mulilo and Oshakati (another transport focus) retained high levels, but so now did the capital at Windhoek and the main port at Walvis Bay. By 1996 Aids was Namibia’s largest single cause of death. A relatively wealthy African country with great mobility, extreme income inequality, little female opportunity, and high levels of sexually transmitted diseases, it had many of the same conditions for epidemic expansion as Botswana.40 Mozambique, by contrast, followed more the patterns of poor countries like Malawi and Tanzania, once its civil war ended in 1992. Many returning refugees were probably infected and especially high prevalence existed on the north-western border with Malawi and in the central region along the Zambezi valley, long garrisoned by heavily infected Zimbabwean and Mozambican troops. In Maputo, antenatal prevalence rose between 1994 and 2002 from 3 to 19 per cent.41
Meanwhile South Africa experienced the world’s largest epidemic, with perhaps 5.3 million infected people in 2003.42 Not only did the socio-economic structures of Apartheid make the country an almost perfect environment for HIV, but the beginning of the epidemic coincided with the township revolt of the mid 1980s and its peak took place a decade later during the transition to majority rule, which compelled ordinary people to concentrate on survival and distracted both the outgoing regime and its nationalist successor from making HIV their chief priority. Yet it would be naive to think that even the most vigorous, stable, and popular government could have protected South Africa from a major epidemic. A contrast is sometimes drawn with Thailand, where an epidemic also became established during the early 1990s but was contained by 1999 at an adult prevalence of 2.2 per cent, whereas South Africa’s was 19.9 per cent.43 Yet this is to ignore the totally different ways in which HIV struck the two countries. Thailand was the first seriously affected country in South-East Asia, with no established epidemic on its borders and a disease that first took root among core groups of drug users, sex workers, and their clients, who could be targeted with impressive energy.44 South Africa, by contrast, bordered a massive continental epidemic and, as will be seen, had no identifiable core group but a great diversity of cross-border contacts that can scarcely now be traced. Of course, better political leadership could have reduced the impact of HIV, but trying to prevent the extensive infection of South Africa would have been like sweeping back the ocean with a broom. Thanks to its uniquely long, asymptomatic incubation period, HIV-1 could probably never have been prevented from reaching epidemic proportions once established in a general heterosexual population. That happened not in South Africa but ten years earlier and 2,500 kilometres away in Kinshasa.
All this is clear from the way the South African epidemic began. The first diagnosed case, in 1982, was in a white, homosexual air steward who had probably contracted the disease in New York and died of the Pneumocystis carinii pneumonia common among American patients. ‘Gay plague hits South Africa’, the Johannesburg Star trumpeted.45 Blood specimens from 200 homosexual men in Johannesburg in 1983 later showed that 32 were already infected. Although homosexuality was technically illegal in South Africa and a taboo subject among respectable Afrikaners, clinics were opened at major hospitals, injecting drug users were screened (and found negative), patients organised their own protection and care, and by 1990 the homosexual epidemic was already levelling off. Of 308 Aids cases reported in South Africa by January 1990, 207 had been in homosexuals, 195 of them white.46 Their infection was not transferred to the general heterosexual population, for the strain of HIV-1 infecting American and South African homosexuals, subtype B, scarcely appeared among heterosexuals until the mid 1990s and then remained rare. By the early 2000s adult prevalence among whites was barely one-third of that among Africans.47
While the medical authorities concentrated on the epidemic among white homosexuals, more perceptive doctors realised that a more dangerous heterosexual epidemic threatened. The first African in South Africa definitely known to have suffered from HIV was a man from the DR Congo who apparently sought treatment early in 1985. During that year 522 blood specimens from Africans in Johannesburg were tested and all found negative.48 The first serious alarm emerged in 1986, when tests on African mineworkers found only 0.02 per cent prevalence among South Africans but 3.76 per cent among men from Malawi. ‘In the compounds and at work we were taunted and heckled,’ the Malawians complained, ‘. . . they called us dying people.’ The government ordered compulsory screening of migrant workers, but trade unions, medical officers, and the Malawian authorities all resisted until all recruiting there was abandoned.49 Such Central African migrants certainly helped to introduce the disease. Two of the first black South Africans known to have contracted HIV were infected some time before 1986 by a Malawian mineworker. The only positive case among 240 African women tested in Johannesburg early in 1987 was a Malawian migrant. But none of the 94 ‘self-confessed promiscuous women’ and 1,065 other women in mining areas tested in 1986 was infected and mineworkers did not become a core group spreading infection to the rest of the South African population, whose prevalence levels they generally shared.50 Nor were sex workers an early focus of disease on the scale of Kigali, Nairobi, and Addis Ababa. By the late 1990s they were often heavily infected – 60 per cent in the Hillbrow area of Johannesburg, 56 per cent at truck stops in the Natal Midlands – but this was not the case earlier in the decade and professional sex workers were rare in African townships, where men seldom blamed infection on them.51
The lack of a core group is a striking feature of the initial infection of black South Africans. The infection was rapid: during 1987 blood screening suggested that HIV prevalence was already eight times higher among blacks than whites and was doubling every six months.52 But it was infection by diffusion across a long, much-permeated northern frontier and through individual contacts in many sectors of a mobile, commercialised environment. One indication of this is that even by 1992 the strains of subtype C virus overwhelmingly dominant in the African population were drawn from all parts of Central Africa, with a large element from neighbouring Botswana, in contrast, for example, to the homogeneity of strains in Ethiopia. Among pregnant women who tested positive at Baragwanath Hospital in Soweto in 1991, ‘A strong link was made with African countries to the north of South Africa or partners who travelled.’
Another indication of the complexity of transmission was that the highest HIV prevalence at that time was not in the industrial heartland of the Witwatersrand but in KwaZulu-Natal.53 Among the likely reasons for this predominance, which continued throughout the 1990s, were the region’s dense rural population, the unusually close interaction between the countryside and the major city of Durban, high rates of mobility and migration, equally high levels of sexually transmitted diseases, and the fact that Zulu had abandoned circumcision two centuries before. Even in 1990 some of the province’s highest prevalence rates, over 3 per cent of adults, were in rural areas crossed by truck routes to Swaziland and Mozambique, with concentrations among late teenage women and those who had recently shifted residence. A study there a decade later found that couples with a migrant male were nearly twice as likely to have one or more member infected with HIV than were couples without a migrant, but that in 29 per cent of couples with only one infected member, that member was the woman. Antenatal prevalence at that time in the northern Umkhanyakude rural district was 41 per cent, against 32.5 per cent for the province and 22.4 per cent for South Africa as a whole.54 The current incidence of new infections among women aged 15–49 at Hlabisa, the region’s main hospital, was 17 per cent a year, as high a figure as was recorded anywhere in Africa during the epidemic. The disease was closely associated with tuberculosis, which had been suppressed during the 1950s by chemotherapy but now became the chief opportunistic infection in HIV-positive patients.
