In Rakai district, similarly, a computer simulation suggests that the annual incidence of new infections among people aged 15–24 peaked in 1987 at about 8.3 per cent.24 Two years later, prevalence among men and women aged over 13 varied from 26 and 47 per cent respectively in main-road trading centres to 22 and 29 per cent in local trading village and 8 and 9 per cent in agricultural villages. In 1990–2, 31 per cent of all households in Rakai district contained an infected member. The worst impact was in the truck-stop towns along the trans-African highway between Kampala and Kigali, notably Lyantonde, where HIV was found in 67 per cent of the bar girls tested in 1986 and in 53 per cent of the entire adult population in 1989.25
The prominence of the trans-African highway was one indication that the epidemic had by the mid 1980s spread far beyond the west lake region. Three categories of mobile men appear especially to have carried it. One was the military: General Amin’s soldiers retreating from the infected border region in 1978–9, Tanzanian troops pursuing them through western and northern Uganda, and Ugandan forces seeking to repress rebellion in the north and east during the 1980s. The northern Gulu district, the chief source of Amin’s troops, recorded 15 per cent prevalence among pregnant women in 1987 and probably became the main route by which HIV entered the southern Sudan and was carried northwards by soldiers and refugees to Khartoum, where in 1998–9 nearly half of those infected had the D subtype found in Uganda and DR Congo.26 The western Ugandan districts of Kabale, Kasese, and Kabarole, prominent in early Aids returns, may also have been infected initially by rival armies. Military actions during the 1980s in Luweero and Soroti districts, further east, were probably important in spreading the disease there.27
A second group carrying the virus were long-distance drivers who infected or were infected by bar girls at their overnight stops in towns like Lyantonde. One study of 68 drivers in Kampala in 1986 reported that 35 per cent already had HIV.28 The third occupational group, with a more diffuse and less certain impact, were migrant labourers carrying the disease to rural homes. ‘With the AIDS pandemic,’ a hospital in the remote south-west of Uganda reported in 1991, ‘it is still the returnees to Bufumbira that introduce this deadly disease into the population which otherwise knows no promiscuity. Among the returnees are also counted the taxi drivers and the long-distance truck drivers.’29
Kampala held a special position. In retrospect, its main prison may have held cases as early as 1979 or 1980, when patients with aggressive Kaposi’s sarcoma also appeared in the main Mulago Hospital, soon followed by others with the chronic diarrhoea and wasting of Slim disease.30 Nobody linked these infections to the emerging Aids epidemic elsewhere in the world until late in 1984, by which time HIV was already entrenched in the city and spreading rapidly. ‘It all started as a rumour,’ the chief epidemiologist later reflected. ‘Then we found we were dealing with a disease. Then we realised that it was an epidemic. And, now we have accepted it as a tragedy.’31 Studies of prevalence among pregnant women in Kampala showed 11 per cent in 1985, 14 per cent in 1986, 24 per cent in 1987 – then the highest figure in the world outside Kigali – and a peak of over 30 per cent in 1989.32 Notably, however, Kampala’s epidemic was not focused on a core group of sex workers and their clients, in contrast to other East African cities. There was little association between HIV infection and commercial sex, which was unorganised, diverse, illegal, and impossible to distinguish from other sexual relationships involving gifts.33 Instead, Kampala’s sexual pattern was closer to Kinshasa’s, with more young women than young men, sexual debut at an average age of fourteen in Uganda generally in 1989, 69 per cent of men and 74 per cent of women aged 15–19 having sexual experience, a rising age at marriage, and many young women whose dependence on gifts from male lovers had been accentuated by the economic disorder of the 1970s and 1980s.34 It was a pattern vulnerable to HIV but capable of change.
Although reports of a novel disease in Rakai reached the authorities in 1982–3, Uganda was then in the midst of civil war and no action was taken until Lwegaba’s report coincided late in 1984 with laboratory evidence that patients at Mulago Hospital with Kaposi’s sarcoma were infected with HIV. Milton Obote’s government, then in power, ordered an investigation. A team visited Masaka, conducted examinations at Mulago, and concluded that Slim was ‘part of the spectrum’ of Aids, although with opportunistic symptoms specific to East Africa. Ruling out transmission by casual or indirect means, the researchers blamed heterosexual promiscuity, perinatal transmission, and blood transfusion, estimating that Mulago Hospital might be creating two new cases each day. HIV-positive patients at Mulago reported on average twice as many sexual partners as HIV-negative patients. Another risk factor was a sexually transmitted infection, especially genital ulcer disease.35
Uganda’s HIV epidemic appears to have peaked in 1991, when 21.1 per cent of women attending antenatal clinics tested positive and some 1,200,000 people were thought to be infected.36 By then the virus had reached almost all parts of East Africa. In Tanzania, the area first affected after Kagera was probably Dar es Salaam. An expatriate may have contracted the disease there as early as 1980, but the first firm evidence was a prevalence of nearly 2 per cent in stored blood collected from pregnant women and blood donors in 1984–5. Thereafter antenatal prevalence in the city rose to 8.9 per cent in 1989 and 14.8 per cent in 1997.37 The disease was probably introduced from Kagera, perhaps by returning soldiers but more probably by Haya sex workers and bar girls from the region, who had been prominent throughout East Africa since the interwar period, driven perhaps by male control of land and income in a highly commercialised region. By 1986, 29 per cent of Dar es Salaam’s bar girls had HIV, with a prevalence of 35 per cent among the 33 per cent of them who came from Kagera. Two years later, 60 per cent of notified Aids patients in Dar es Salaam originated from Kagera, many of them no doubt people seeking treatment. Of Tanzania’s first 212 notified Aids cases, 60 per cent of males and 46 per cent of females said that they were heterosexually promiscuous.38 Yet this initial social profile was soon obliterated by the epidemic’s expansion. When women at family planning clinics in Dar es Salaam were surveyed in 1991–2, there was still a positive association between HIV infection and number of sexual partners, but even infected women had a median of only two partners within the previous five years, while married women claiming fidelity to husbands had a significantly greater risk of infection if the husband had not been faithful, a risk that increased with the woman’s own education and her partner’s.39
Dar es Salaam was a thousand kilometres from Kagera and almost as remote from Tanzania’s other borders, yet by August 1986, less than two years after HIV was recognised in the capital, its main hospital had admitted cases from each of mainland Tanzania’s twenty regions. Some were probably infected from Dar es Salaam. In 1988 the highest prevalence, after Kagera, was in Iringa region on the Tanzam road linking the capital to Zambia.40 Other areas, by contrast, acquired HIV by cross-border contact. In the south-western Mbeya region, for example, an explosive HIV and tuberculosis epidemic between 1986 and 1994 was caused by the C subtype of HIV-1, probably introduced from Zambia to the south and most prevalent at the border and in urban and roadside locations.41 Mwanza region, south of Lake Victoria, was probably infected from Kagera, but Mara region, on the eastern shore of the lake, appears to have shared the severe epidemic in the neighbouring Nyanza province of Kenya. In the Kilimanjaro and Arusha regions of northern Tanzania the disease was blamed on young, mobile traders returning from Kagera, Dar es Salaam, and Kenya. As everywhere in the continent, the epidemic there took its shape from the structure of the commercial economy, with a focus among urban bar girls and sex workers, high infection among young adults driven from fertile mountainsides by land scarcity, and prevalence declining as the disease radiated out into the countryside. In Arusha region in 1992, for example, adult infection was 10.7 per cent in the poorer parts of the regional capital, 5.2 per cent in the wealthier parts, 2.2 per cent in semi-urban areas, and 1.6 per cent in the countryside, where at this time the disease was still seen as a complaint of despised urban aliens.42 Because HIV entered Tanzania from all directions, the country had an unusual diversity of subtypes and