‘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.
6
The Penetration of the West
The penetration of HIV-1 from the equatorial region into West Africa differed markedly from its expansion to the east and south. Except in Côte d’Ivoire, it was more gradual and less complete, reaching in the early 2000s prevalences only one-fifth or one-sixth of the highest elsewhere. The reasons for this are unclear but probably include obstacles to overland mobility from east to west, the wider economic opportunities open to West African women in towns, widespread male circumcision, relatively low HSV-2 prevalences, and the barriers to infection presented by Islamic moral and marital patterns. Another difference, of less certain relevance, was that when the HIV-1 virus entered West Africa, it found HIV-2 already established.
As a human disease, HIV-2 was probably older than HIV-1. It was closely related to the simian immunodeficiency virus found in sooty mangabey monkeys (SIVsm) living only in the West African forest region between the Casamance River in Senegal and the Sassandra River in Côte d’Ivoire, which was also the endemic location of the human virus. HIV-2 shared some 70 per cent of its genome with SIVsm but only about 42 per cent with HIV-1. Indeed, some of the eight groups of HIV-2 known in 2004 were more like SIVsm than they were like one another. This was because SIVsm was very widespread and diverse (although completely harmless) in sooty mangabey monkeys and because each HIV-2 group was probably the result of a separate transmission from a monkey.1 Of the eight groups, six had failed to establish themselves in human beings, having infected only seven known cases between them. Of the two more successful, group A was the more common throughout the coastal region west of Côte d’Ivoire, while group B was found chiefly in Côte d’Ivoire and Ghana, although scattered cases of both existed elsewhere.2 A study using molecular clock techniques estimated that the most recent common ancestor of group A existed in 1940±16 and of group B in 1945±14.3 Yet, given the high prevalence of SIV among sooty mangabeys, their close interaction with human beings, and the frequency of twentieth-century transmissions, similar transmissions had probably taken place in earlier centuries.
This was more likely with HIV-2 than HIV-1 because HIV-2 was a less virulent and visible disease in human beings, possibly because its progenitor was so fully adapted to monkeys. HIV-2 was about three times more difficult than HIV-1 to transmit through sexual
