Читать книгу The African AIDS Epidemic - John Iliffe - Страница 13

5

The Conquest of the South

The countries of southern Africa, although infected with HIV slightly later than those further north, nevertheless overtook eastern Africa’s levels of prevalence during the mid 1990s and then experienced the world’s most terrible epidemic. By 2004 the region had 2 per cent of the world’s population and nearly 30 per cent of its HIV cases, with no evidence of overall decline in any national prevalence, which in several countries exceeded 30 per cent of the sexually active population. The chief issue in southern Africa is therefore to explain the speed and scale of epidemic growth. The obvious explanation is the region’s history of white domination and the dramatic economic change and social inequality it had wrought. The view here is that this is true, but the connections were not always obvious, while, as everywhere in Africa, the scale of the epidemic was chiefly due to the long incubation period that enabled it to spread silently beyond hope of rapid suppression.

By chance, both the earliest definite indication of HIV in southern Africa and the best evidence of the silent epidemic anywhere in the continent come from the remote rural Karonga district of northern Malawi, bordering Tanzania and Zambia. Karonga’s people, famed in colonial times for their education received from Scottish missionaries, had migrated as clerks and craftsmen throughout the industrial centres of southern Africa. This may first have exposed them to HIV. The virus’s arrival in Karonga can be traced because the district experienced a mass campaign against leprosy and tuberculosis that included two total population surveys, in 1981–4 and 1987–9, each of which took and stored blood specimens from everyone in two sections of the district. All 44, 150 specimens have been tested retrospectively for HIV, although only those from people aged 15–49 are included in the calculations. The results give a uniquely detailed picture of the dynamics of a local epidemic.¹

In the first round of investigation, none of the 1,041 specimens taken in 1981 had HIV. Four infected specimens were taken in 1982, one in 1983, and six in 1984, making a total of eleven in 12,979 specimens, or less than 0.1 per cent. Four were men and seven women. Eight were recent arrivals in the district: four from other parts of Malawi (including the main city, Blantyre), two from Tanzania, and two from Zambia. Not only was the disease brought from several outside sources almost simultaneously, but several different subtypes were introduced. The two arrivals from Tanzania brought subtypes A and D, the two forms dominant in East Africa. Of the other nine specimens from this period, six were later identified as subtype C, while the other three could not be positively identified but were closest to subtype C and possibly an extinct variety of it.

Map 3 Southern Africa

Of the six individuals definitely identified with subtype C, one came from Zambia, two had been born in Zambia but had lived in Blantyre, two had come from elsewhere in Malawi, and one was a long-term resident of Karonga. Subtype C was to dominate the southern African epidemic, causing some 94 per cent of infections there in 2001.² It may have originated in the southern DR Congo,³ which had many links with neighbouring Zambia, especially through the mining towns of Katanga and the Zambian Copperbelt. A possible reconstruction, compatible with evidence of early infection elsewhere in Malawi and Zambia that will be quoted later, is that elements of the East African epidemic (subtypes A and D) spread across the border into rural Karonga, but that the bulk of infection (subtype C) was carried from the southern DR Congo into Zambia, probably first to the Copperbelt, spread to other urban centres (including Blantyre) by 1983, and was carried from these centres into Karonga. Something can even be known of the process of infection. Of the six specimens with subtype C, four were so closely related genetically as to form a single cluster (cluster 1) with a single origin. One of the four was the long-term resident of Karonga. The other three had come from other parts of Malawi. The most likely scenario is that one person introduced the strain from elsewhere in Malawi and infected the other three after arriving in Karonga, although this cannot be certain.

Cluster 1 becomes central when attention shifts to the second round of blood collection in 1987–9. This revealed not 11 but 189 HIV-positive specimens, a prevalence of 2 per cent. Of the 168 specimens that could be analysed by subtype, 152 (90 per cent) belonged to subtype C, 6 to D, 3 to A, 3 were unclassified, and 4 were recombinants. Not only had subtype C established itself as the dominant form, but so had cluster 1: 40 per cent of those with subtype C (61 people) were infected with variants of that strain, probably introduced no more than five or ten years earlier by a single individual. Nothing could illustrate more vividly the explosive potential of a virus whose existence in their bodies was almost certainly unknown to most of those harbouring it.

The data collected in 1987–9 reveal much more about HIV epidemiology in Karonga. A majority of those infected were women, with an especially rapid increase in the late 1980s among women aged between 15 and 24, whereas men with HIV were generally older. Some 87 of the 189 infected people had not been present in the district in 1981–4, divided between 48 returning absentees and 39 new immigrants. Clearly the epidemic was still driven chiefly by mobility beyond the district. Prevalence increased with years of schooling and was most common among traders, salaried employees, casual labourers, and generally those who were not peasant farmers. Those with the best and the worst housing had higher prevalence than those with houses of intermediate quality. Of eighteen couples in which both partners were infected, only twelve were infected with closely related viral strains. Most intriguing was the dominance of subtype C, for one unanswered question about the epidemic is whether this subtype, which by the 2000s was responsible for more than half the world’s HIV infections, had greater evolutionary fitness than other subtypes. Despite much research and several detailed differences in its mode of operation, no conclusive evidence of this had emerged by 2005, although one study had shown that viral concentrations were more than three times as high in the blood and semen of Malawian men, over 90 per cent of them with subtype C, than in Americans with subtype B.⁴

Although the data from Karonga are uniquely detailed, it was clearly not the first part of Malawi to experience HIV infection. Study of stored blood taken in southern Africa before 1974 has revealed no evidence of HIV, but the first 17 Aids cases were reported from Malawi’s health facilities in 1985, some with aggressive Kaposi’s sarcoma, and a year later nearly 4 per cent of Malawian mineworkers in South Africa were HIV-positive, the only national group from Central Africa significantly infected. Given the long incubation period before the appearance of symptomatic Aids, and given the wide extent of HIV infection evident by the mid 1980s, Malawi’s silent epidemic probably began before 1980, or only slightly after HIV can be discerned around Lake Victoria. Census data show that mortality in Malawi increased significantly between 1977 and 1987, but chiefly among children, who commonly died of Aids more quickly than adults.⁵

The virus may have reached Zambia slightly earlier than Malawi, although the evidence is indirect. In 1983 Anne Bayley, a surgeon in Lusaka, found herself treating unprecedented numbers of young adults afflicted with aggressive Kaposi’s sarcoma. When tested in 1984, 91 per cent of these were found HIV-positive. Bayley later thought that the first case might date back to 1980 and that HIV had probably reached Zambia in the mid 1970s, initially spreading slowly. She added – a conclusion presumably reached by retrospective testing – that in 1981 fewer than 1 per cent of women at Lusaka’s antenatal clinics were HIV-infected.⁶ Many early patients in Lusaka with Kaposi’s sarcoma had associations with the Copperbelt, where tuberculosis cases suddenly multiplied from 1984 and the first small HIV tests in the general population of mining communities in 1985 showed 13.5 per cent prevalence in males and 21 per cent in females. Of deaths from Aids reported from Zambia between March and July 1987, 46 per cent were from the Copperbelt and 18 per cent from Lusaka.⁷ Yet the situation in the capital was alarming enough, for tests there in 1985 showed that 8 per cent of pregnant women were infected. In February 1986 Aids patients were also dying in Livingstone on Zambia’s southern border with Zimbabwe.⁸

In reality, the silent epidemic had penetrated Zimbabwe some time before, although perhaps three or four years later than Zambia and Malawi as the virus was carried southwards. The first cases of Aids and aggressive Kaposi’s sarcoma were diagnosed in 1983. Alarm arose only when blood was first screened in 1985 and it was revealed that over 2 per cent of donors had HIV. Infection then concentrated in the northern city of Harare, with only 0.05 per cent of donors testing positive in Bulawayo, further south. Thereafter, however, expansion became general and rapid. At the district hospital at Hurungwe in Mashonaland West, the annual number of patients diagnosed with HIV rose between 1986 and 1988 from 16 to 292. In Manicaland province, on Zimbabwe’s eastern border, all districts recorded increased mortality from the late 1980s. By 1990 national antenatal prevalence was 12.9 per cent.⁹

Botswana was invaded next, slightly later than Zimbabwe and just as stealthily. Over 200 blood specimens collected in the north during 1984 showed no HIV. ‘It’s not a problem in Botswana,’ an official declared, ‘AIDS is primarily a disease of homosexuals and there is no homosexual in Botswana.’ The first case reported at that time was indeed a white homosexual.¹⁰ When the first Tswana tested positive a year later, the Minister of Health ‘allayed fears by mentioning that the modes of transmission of the disease means that it could not become a big epidemic’. Within another year, however, he was speaking of ‘a scourge that could decimate a large portion of the human race’ and recommending ‘a stable, faithful relationship with another uninfected person’. By then Botswana had 30 known HIV cases and feared that the real number might be more like 3,000. In 1990 tests showed that 5–7 per cent of blood donors in towns and 1–2 per cent in the countryside were infected.¹¹

During the 1990s these four countries of Central Africa overtook East Africa as the chief focus of the global epidemic. Malawi experienced rapid growth of infection during the later 1980s in the major towns, led by Blantyre where infection rates at the hospital antenatal clinic rose from 2.0 per cent in 1985 to 25.9 per cent in 1991 and a peak of 32.8 per cent in 1996. A small study there in 1990–5 suggested an annual incidence of new infections among women of 4.21 per cent, or perhaps four times the rate during the Kinshasa epidemic. During that period, however, prevalence probably grew even faster in the countryside, narrowing the hitherto wide urban–rural differential. In 1996 adult prevalence was 23 per cent in urban, 18 per cent in semi-urban, and 12 per cent in rural areas. Given that only 12 per cent of Malawians lived in towns, most infections were rural.¹²

By the mid 1990s Zambia’s prevalence had overtaken Malawi’s. According to a later estimate, adult infection peaked in 1994–5 at about 17 per cent. As in Blantyre, the growth of the epidemic in the late 1980s was especially rapid in Lusaka, where antenatal prevalence rose to a roughly stable 22–27 per cent at different clinics in 1990–3. The difference was that 50 per cent of Zambians were urban and that overall prevalence in Copperbelt province almost equalled that in the capital.¹³

Yet Zambia, too, was soon overtaken. Zimbabwe’s prevalence figures are especially difficult to interpret, with wide variations between those quoted by national and international authorities and even wider fluctuations at individual sentinel sites. The most reliable data are probably for antenatal clinic attenders in Harare. Prevalence among them was 10 per cent in 1989 and 18 per cent in 1991, both figures substantially less than in the main cities of Malawi and Zambia, but it grew further to a peak of 32 per cent in 1995 and then fluctuated around that level. Yet only 28 per cent of Zimbabwe’s people were urban.¹⁴ The distinctive feature of its experience during the 1990s was the high level of prevalence outside the main cities, often so high that the statistics must be treated with caution. Three kinds of areas were worst affected. One contained towns on main roads close to borders, where truck drivers might socialise for several days while negotiating their way across the frontier. Beitbridge, on the South African border, recorded 59 per cent HIV prevalence in 1996, while the figure at Mutare, near the frontier with Mozambique, reached 37 per cent in 1997.¹⁵ Second, the trucking routes contributed to high prevalence in provinces and districts through which they passed. Masvingo province, which registered a barely credible provincial figure of 49.4 per cent among pregnant women in 2000, was bisected by the road from Harare to South Africa, while Midlands province, with a reported 45.1 per cent prevalence in 2000, straddled the route from Harare to Bulawayo.¹⁶ Yet this devastating provincial infection that distinguished Zimbabwe was not confined to transport routes but existed even in remote rural areas. In 1993–4 overall adult prevalence was already 24 per cent in the Honde valley, a fairly isolated part of Manicaland. Shortly thereafter, 22 per cent of pregnant women tested HIV-positive even at Tsholotsho in arid northern Matabeleland.¹⁷ As will be seen later, both its excellent transport system and its high levels of oscillating migration between country and town made rural Zimbabwe especially vulnerable to infection.

Those characteristics operated even more powerfully in Botswana. From only 2 or 3 per cent in 1990 its national adult prevalence soared to 23 per cent in 1995 and either 28 per cent (according to the government) or 36 per cent (according to UNAIDS) in 2000, the latter figure being the highest in the world.¹⁸ As the epidemic spread south, its momentum seemed to accelerate, suggesting the possibility that rapid passage of the virus from person to person might be increasing its virulence, although there was no hard evidence of this. The acceleration in Botswana was noticed first not at the capital, Gaborone, but at Francistown, where the main road crossed into Zimbabwe and antenatal prevalence reached 24 per cent in 1992 and 34 per cent in 1993. Gaborone soon followed, as did the mining town of Selebi Phikwe; in 2000 these three towns registered antenatal prevalences of 44, 36, and 50 per cent respectively.¹⁹ Yet this initial urban predominance was reversed as the epidemic grew. By 1999 prevalence among pregnant women was 22 per cent even in the Kgalagadi desert area, while the highest reported prevalence among them at that time was 51 per cent in the northern district of Chobe. Overall, according to the government, ‘the 2002 survey reveals slightly higher rates in rural than in urban areas’. The annual incidence of new infections for the whole country at that time was estimated to be 6 per cent, roughly three-quarters of the level reached among young people at Rakai during the 1980s.²⁰

An early attempt to explain the speed and scale of Botswana’s epidemic highlighted three factors: ‘the position of women in society, particularly their lack of power in negotiating sexual relationships; cultural attitudes to fertility; and social migration patterns’.²¹ Gender inequality fostered the epidemic throughout Central Africa. Commercial sex, driven mainly by female poverty and lack of opportunity, has been little studied in Botswana, but elsewhere it was important especially in initial urban epidemics, although probably less central than in Nairobi or Kigali. Women held only 8 per cent of Zimbabwe’s and 15 per cent of Zambia’s formal sector jobs in the early-mid 1990s.²² ‘Divorce, rural poverty and superior earnings were the principal reasons cited’ by sex workers in Harare in 1989; 70 per cent of them were divorced, probably with children to support, and nearly half came from drought-stricken southern Matabeleland. Six years later, 86 per cent of sex workers tested there had HIV, like 70 per cent of those working the main road between Zimbabwe and Zambia in 1987, 56 per cent in Blantyre in 1986, and 69 per cent in Ndola in 1997–8.²³ Although willing to use condoms, only about half of those in Harare in 1989 and one-quarter of those in Blantyre and Ndola in the mid 1990s could overcome their clients’ opposition.²⁴ Studies of young male factory workers in Harare during the 1990s showed both their fecklessness and their difficulty in avoiding risk where HIV was so widespread. Their annual incidence of new infections was 2 per cent, meaning that half were likely to contract HIV during a normal working lifespan. Similar levels of infection existed among long-distance drivers.²⁵ A Malawian villager later recalled how passing tanker drivers infected local women:

The wives were spreading the virus to their husbands, the unmarried women were infecting the young men, the young men making money from smuggling were going into Lilongwe and having sex there. People were behaving very freely and they had no idea that anything bad could happen to them. . . . By 1996, 12 years after the trucks first started arriving, the death rate in the village peaked at four a week. . . . Our neighbours from other villages would not come to help people who were sick or help at a funeral because of fear of contracting the disease. . . . We became completely isolated.²⁶

More commonly, however, infection passed from promiscuous men to their wives. In one small enquiry in Lusaka, lasting a year, 26 per cent of HIV-positive husbands infected their wives, while only 8 per cent of HIV-positive wives infected their husbands. ‘Men generally acquire infection first,’ a careful study in Manicaland reported, ‘frequently during spells of labour migration in towns or commercial areas, and then pass on the infection to their regular female partners based in rural areas.’ By 1998 twice as many women as men there were infected, including four times as many among people aged 17–24, owing to the disparity of age between sexual partners.²⁷

Nevertheless, women too could be ‘movious’, as Central Africans described it. Most were not: even the highest self-reported accounts of sexual behaviour suggest that only about 25 per cent of women had non-marital sex. Yet of those attending antenatal clinics in two areas of Manicaland in 1993–4, 16 per cent of married women, 43 per cent of single women, and 50 per cent of formerly married women were infected.²⁸ Among the many factors encouraging extra-marital sex, one of the most important was delayed marriage, due chiefly to education, labour migration, and the decline of polygyny. In Botswana in 2001, for example, the median age at first marriage or cohabitation was 28 for men and 23 for women. Consequently, in 1995 over 60 per cent of never-married women aged 20–24 there were mothers, while 41 per cent of boys and 15 per cent of girls aged 15–16 had sexual experience. In Lobatse and Francistown, with very high HIV prevalence, 47 per cent of men and 39 per cent of women aged 17–18 had a casual partner over a twelve-month period; 21 per cent and 16 per cent had at least two. Of teenage girls who bore children in the late 1980s, 40 per cent had them with men six or more years older than themselves. Young Tswana had adopted an experimental attitude towards sex – ‘marketing themselves’ as it was known – ‘so that you can compare them and see who amongst them perfectly suits your life’.²⁹ Many women deliberately avoided marriage in order to maximise their freedom. It made them immensely vulnerable and created an exceptionally wide generation gap between young people and those raised under strong traditional or Christian influence.³⁰

Botswana’s late twentieth-century sexual order originated as an adaptation to education and labour migration.³¹ It was one consequence of the mobility that drove the Central African epidemic, evident in the initial infection of Karonga, in the roles of long-distance drivers and dusty border towns like Beitbridge, and in the migration routes to the Copperbelt or the Nchalo sugar estate in southern Malawi, where the annual incidence of new infections is reported to have reached a brief peak of 17.1 per cent during 1994–5. In Zimbabwe, prevalence at antenatal clinics in 2000 ranged from 26.8 per cent in rural locations to 53.9 per cent in commercial (farming and mining) settings, peaking at 70.7 per cent in Chiredzi, another sugar plantation area.³² HIV thus followed the pattern of the commercial economy, straddling the urban–rural divide that checked it in Ethiopia. In each Central African country there was a close relationship between patterns of infection and of oscillating labour migration. Botswana experienced rapid urbanisation – Gaborone’s population multiplied more than ten times between 1971 and 1997 – but nevertheless had higher rural than urban prevalence of HIV because its people held to a long tradition of maintaining separate homes in towns and the countryside, between which they had in the past oscillated at different seasons, a practice now facilitated by motor transport. In Zimbabwe a similar oscillating pattern had grown up in the colonial period as men maintained land rights and families in the communal reserves while working in mines and cities. This, it has been argued, raised rural HIV prevalence close to urban levels.³³ Colonial Zambia had known a similar pattern of mobility, but its severe economic decline after 1974 made towns less attractive and travel to distant provinces more difficult, so that the urban–rural differential in HIV prevalence was wider than in Zimbabwe, although narrower than elsewhere. Malawi, a poorer country, initially had much higher levels of infection in Blantyre and Lilongwe than in the countryside, but the contrast narrowed during the 1990s, partly perhaps in the natural course of epidemic development but also because economic decline drove infected young people into the countryside.³⁴

Botswana’s epidemic was fuelled also by ethnic and cultural homogeneity, facilitating social interaction, and by its new-found diamond wealth, which gave it the world’s highest economic growth rate during the last third of the twentieth century. Yet, as its citizens said, Botswana was ‘a rich country of poor people’, 47 per cent of them living below the poverty line in 1993–4. Such polarisation fostered both risk taking in the rich and vulnerability in the poor.³⁵ In Karonga those first infected had been the more prosperous and educated, but as the epidemic developed it focused increasingly on the poor. A survey of mining and industrial workers in Zambia, Botswana, and South Africa in 2000–1 showed HIV prevalence ranging from 4.5 per cent among managers to 10.5 per cent among skilled workers and 18.3 per cent among the unskilled.³⁶ In addition to driving women into vulnerable occupations, poverty fostered disease by weakening medical systems and putting treatment beyond the reach of the poor. Between 1980 and 2000 the number of notified tuberculosis cases in Zambia, Zimbabwe, and Malawi multiplied five times as a result of HIV infection and decaying health systems.³⁷ Although sexually transmitted diseases declined during the early years of the HIV epidemic, owing to wider use of condoms and greater emphasis on treatment, they were increasingly supplemented by HSV-2, which spread in synergy with HIV to infect 40 per cent of sexually active men and 61 per cent of sexually active women in Ndola in 1997. The lack of male circumcision in Central Africa added to the risk of HIV infection. In Botswana, ironically, circumcision had largely been abandoned during the twentieth century.³⁸

While the epidemics in Malawi, Zambia, Zimbabwe, and Botswana reached maturity during the late 1990s, those in Mozambique and Namibia were still explosive. In both countries the warfare of the 1980s appears to have checked the spread of HIV by obstructing normal mobility. In Mozambique a study in ten provincial capitals in 1987 found average adult prevalence of 3.2 per cent, while in Maputo, isolated on the southern coast, antenatal prevalence was still less than 1 per cent in 1990.³⁹ In Namibia, similarly, only 4.2 per cent of 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. Tuberculosis cases at Hlabisa multiplied nearly six times between 1990 and 2001. ‘The country,’ wrote the doctor in charge, ‘is busy burying its young.’⁵⁵

The peak expansion of South Africa’s HIV epidemic lasted from about 1993 to 1998, when the number of new cases began to decline.⁵⁶ Apart from KwaZulu-Natal, the worst-affected provinces were Gauteng, the Free State, and Mpumalanga, but perhaps the most severe impact was in the independent states of Lesotho and Swaziland, both tied to South Africa by labour migration. The mines were not initially major centres of infection and HIV only slowly penetrated Lesotho. Its statistics are particularly erratic, but prevalence appears to have been low until 1993, when a dramatic increase took place, reaching 31 per cent at urban antenatal sites in 2002. The carriers were returning mineworkers – 48 per cent were estimated to be infected in 2000 – who transmitted the virus to the women who in 2002 were 55 per cent of those infected.⁵⁷ Swaziland was less dependent on migration to South Africa, but there, too, rapid infection coincided with the acceleration of the South African epidemic around 1993. A year later, 16 per cent of antenatal clinic attenders were HIV-positive and the proportion increased continuously thereafter to nearly 39 per cent in 2003, a figure rivalled only in Botswana. Rural and urban prevalences were almost the same. This rapid, sustained, and widespread growth was probably driven chiefly by mobility within Swaziland and the particular subordination of young women.⁵⁸

Within South Africa, similarly, high levels of mobility ensured that infection was relatively evenly distributed between town and country. In 2002 the first population survey found 12.4 per cent adult prevalence in African rural areas, 11.3 per cent on commercial farms, and 15.8 per cent in areas of formal urban housing, but a markedly higher prevalence (28.4 per cent) in ‘informal urban areas’, the squatter settlements ringing every town.⁵⁹ This was the most striking evidence anywhere in Africa that the epidemic had come to concentrate among the poor. One connection was the prevalence of sexually transmitted diseases which were roughly three times as common in informal housing areas as elsewhere. An intensive study in the Carletonville mining area of Gauteng in 1999 found that HSV-2, the main cause of genital ulcers, was the single best predictor of HIV, infecting 91 per cent of HIV-positive women and 65 per cent of HIV-positive men aged 14–24. Among men at an STD clinic in Durban, similarly, HIV prevalence increased between 1991 and 1998 from 5 to 64 per cent and HSV-2 prevalence rose from 10 to 41 per cent.⁶⁰

A second connection between HIV and poverty concerned gender relationships. While commercial sex was relatively unimportant in the townships, widespread partner exchange like that in Kinshasa and Bangui was markedly more common among the young there than in other contexts.⁶¹ Among men it was in part inherited from a polygynous tradition, but it was due also to the collapse of rural restraints on premarital sex (especially its restriction to non-penetrative intercourse), to artificial contraception that reduced the risk of unwanted pregnancy, to the disempowerment of poor young men who could not afford to marry and establish households, and to a reactive machismo that was further stimulated by the violence of the anti-Apartheid struggle.⁶² Although observers overdramatised the ‘lost generation’ of the early 1990s, many young townsmen of the time aspired to be an isoka, the handsome, popular, and irresponsible hero who displayed his masculinity, in one of the few ways available in a township, by having penetrative sex with girlfriends whom he could not afford to marry. ‘If I were to have many lovers,’ one explained, ‘people . . . would think that I was a playboy, which is a very nice thing to be.’⁶³ Sexual debut came increasingly early, at a median of perhaps sixteen years. Condoms were despised as destroying both pleasure and trust. Many young men had little sense of their own danger: as late as 2003, 62 per cent of HIV-positive people aged 15–24 believed they were at little or no risk of infection. Others accepted the risk as one among many that they faced. ‘We thought that with the new government we could relax, study, plan a future,’ a man of twenty said in the mid 1990s. ‘Now AIDS is here to give us no future, Well, we’ll all just get it and that’s life. We’re cursed; we really are the lost generation.’⁶⁴

For young township women, the danger could be more immediate. Of those aged 14–24 interviewed at Carletonville in 1999, 16 per cent had been forced to have sex against their will. Perhaps 2 per cent of women of childbearing age were raped each year. These were only the most blatant forms of coercion. More took the form of steady pressure rather than violence. Many men and women believed that a man who had given bridewealth for a woman, spent money on her, or received encouragement from her had a right to sex regardless of her wishes: ‘Once you have kissed each other that means you are preparing for sex. If she refuses at that point you must just force her.’⁶⁵ Not all needed to be forced. For some poor young women, their sexuality might be their only means of survival or of acquiring coveted goods and other benefits. A study in Cape Town found that about 20 per cent of teenage women reported sex for money or presents. ‘If he wants a woman like me, a man must pay,’ one said. ‘Forget about marriage . . . that was something for our mothers and grannies, it’s not for us.’⁶⁶ Yet even young women eager to be regte, steady girlfriends with hope of marriage, were equally at risk of infection, for it commonly implied unprotected sex. In the mid 1990s one-third of South Africa’s teenage women bore a child. Ten per cent of these women had HIV. By the age of 25, one-quarter would be infected.⁶⁷

In its silent origins, its rapid expansion, its association with mobility, its exploitation of gender inequality, and its growing concentration among the poor, South Africa’s epidemic was an extreme version of a continental pattern, much as Apartheid had been an extreme version of a wider colonial order. The epidemic that had begun two decades earlier close to the equatorial forest had culminated at the southern extremity of the continent. From that extremity the counter-attack would eventually begin.