number of deaths. The missing element in the story, however, was expansion to the countryside, for the remarkable point about Ethiopia – in contrast, say, to Nyanza – was how little impact the disease had made in rural areas, where estimated adult prevalence was 0.3 per cent in 1990 and 0.8 per cent in 1995. This was partly misleading, for such was the predominance of the countryside in Ethiopia – 83 per cent of the population in 1999 – that rural infections overtook urban from 1997. Yet rural prevalence in 2000 was still only an estimated 1.9 per cent. It was highest in the central Amhara region, but in the remote Southern Nations Nationalities and Peoples Region, at that date, only 37 per cent of women had even heard of Aids, although the impact grew rapidly thereafter.69 Rural people, there and elsewhere, blamed townsmen and foreigners for the disease: ‘We Hamar don’t have cars with which to reach America. We don’t go to England, to gal [highland] country, to Germany, and going there, we don’t come back bringing illness. It comes to us by foot.’70
As in Rwanda and Burundi, it is difficult to explain the weakness of urban–rural transmission of HIV in Ethiopia during the 1990s. One element may have been the dispersed pattern of rural settlement that limited interaction. Studies of the extent to which farmers frequented sex workers in market towns found inexplicably varied proportions.71 As in Rwanda, occasional visits might do little to spread a virus so difficult to transmit, especially in a culture with near-universal male circumcision. The most detailed rural study, of a Muslim area in eastern Hararghe, concluded that it was protected from infection by its Muslim social order and its lack of exposure to high-prevalence urban groups.72 Perhaps this last point was the most important. The HIV/Aids epidemic throughout eastern Africa had been shaped by the network of communication provided by commercial economies. Vigorous around Lake Victoria and along the trans-African highway, they were less integrated in Rwanda and Burundi or the emptiness of central Tanzania. The particular weakness of its commercial economy had shaped much of Ethiopia’s modern history, notably its uncompleted revolution. Now the same circumstances helped to protect its countryside against infection.
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
