The earliest convincing evidence of the human immunodeficiency virus (HIV) that causes the acquired immune deficiency syndrome (Aids) was gathered in 1959 amidst the collapse of European colonial rule in Africa. In January 1959 rioters briefly seized control of the African townships of Leopold ville, the capital of the Belgian Congo, shocking its rulers into frantic decolonisation. In the same year an American researcher studying malaria took blood specimens from patients in the city. When testing procedures for HIV became available during the mid 1980s, 672 of his frozen specimens from different parts of equatorial Africa were tested. Only one proved positive. It came from an unnamed African man in Leopoldville, now renamed Kinshasa. The test was confirmed by the Western Blot technique - generally considered the most reliable method - and by different procedures in three other laboratories. Although nothing of this kind can be absolutely certain, there are strong grounds to believe that HIV existed at Kinshasa in 1959 and that it was rare.
One importance of the Kinshasa case is to establish a date by which HIV existed, but in itself the case does not imply that the Aids epidemic began in western equatorial Africa. If that unnamed African had been the first person ever infected with HIV, it would have been an incredible coincidence. Once Aids was recognised as a medical condition early in the 1980s, researchers found several early accounts of patients whose recorded symptoms had resembled it. Luc Montagnier, whose laboratory first identified HIV, thought that the earliest case had been an American man who died in 1952 after suffering fever, malaise, and especially the Pneumocystis carinii pneumonia that afflicted later American Aids patients, but no blood had been stored for later testing and the symptoms demonstrated only suppression of the immune system, for which there could have been reasons other than HIV. The same was true of a Japanese Canadian who died in 1958 and a Haitian American in 1959. More convincing was the case of a fifteen-year-old, sexually active American youth who died in 1969 with multiple symptoms including an aggressive form of Kaposi's sarcoma, a tumour common in later Aids patients.
Although it is unlikely that the world's first HIV epidemic in a general heterosexual population could have been prevented from causing terrible suffering, it is also true that the measures taken by national and international authorities during the 1980s and 1990s were generally considered inadequate. Most African governments were slow to grasp the scale of the crisis, because many were weak regimes faced with more immediate problems, the crisis was itself so novel, and they perceived a threat to the national dignity that they had so recently asserted. Consequently, the first epidemic did not produce the first response. When African regimes did eventually react, they found that the Western powers dominating international affairs had already defined strategies designed to tackle their own less threatening epidemics. These strategies, propagated by the World Health Organisation in one of the most striking modern examples of globalisation, proved less effective in Africa. Whether any other strategy could have been more effective, especially in the earlier stages of the epidemic, remains uncertain.
The Western strategy was designed to counter epidemics in stigmatised but articulate minorities of homosexuals and injecting drug users. The crux was to avoid demonising and isolating these minorities, win their voluntary cooperation, persuade them individually to abandon high-risk behaviour, collaborate with them in caring for the infected, and educate the wider public to avoid infection. HIV was not to be treated like the epidemic diseases of the past, which Western societies had not experienced for sixty years, but like the dominant degenerative diseases of the time, such as cancer. This strategy fitted smoothly into the liberal, doctor-dominated health and sexual policies of Britain and France. It worked less smoothly in the United States, where doctors had less control over public policy, the Reagan administration did not conceal its distaste for deviant minorities, and militant homosexual groups defended their interests in the name of human rights. The effect, however, was largely the same: by 1986-7 Western Aids policies were firmly voluntaristic and sensitive to the rights of the individual patient, with a relative unconcern for the protection of the uninfected because infection was concentrated among minorities and easy to avoid.
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.
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.
This book has a modest purpose. Many history students interested in Africa wish to study the HIV/Aids epidemic but are hampered by the lack of an introduction to the detailed literature. This book is intended as an introduction, for students and other readers.
The book is not a work of research. A thorough history of the epidemic during its first thirty years would demand fieldwork in affected communities, interviews with those involved, and study of unpublished records of international organisations, national governments, and private individuals. I have not attempted any of these, nor have I the necessary medical and anthropological skills. Instead, the book is a synthesis of the more important and accessible published material, put into a historical form.
A historical account offers four advantages. First, it suggests an answer to the question posed most provocatively by President Mbeki of South Africa: why has Africa had a uniquely terrible HIV/Aids epidemic? Mbeki attributed this to poverty and exploitation. Some earlier analysts suggested that Africa had a distinctive sexual system. This book, by contrast, stresses historical sequence: that Africa had the worst epidemic because it had the first epidemic established in the general population before anyone knew the disease existed. Other factors contributed, including poverty and gender relationships, but the fundamental answer to Mbeki's question was time. Like industrial revolutions or nationalist movements, Aids epidemics make sense only as a sequence.
Second, a historical approach highlights the evolution and role of the virus. Because HIV evolves with extraordinary speed and complexity, and because that evolution has taken place under the eyes of modern medical science, it is possible to write a history of the virus itself in a way that is probably unique among human epidemic diseases. At the same time, the distinctive character of the virus - mildly infectious, slow-acting, ineradicable, fatal - has shaped both the disease and human responses to it.
Third, many aspects of the epidemic come into focus only when seen in the longer context of African history. Although HIV/Aids was profoundly different from earlier African epidemics, it arose from the human penetration of the natural ecosystem that is the most continuous theme of the African past.
This book began by suggesting that a history of the African HIV/Aids epidemic to 2005 could offer four valuable perspectives. One was an answer to President Mbeki's question why Africa had suffered the most terrible epidemic. The book has argued that the presence of the natural ancestor of HIV and the full range of viral subtypes in the western equatorial region of Africa is compelling reason to believe that the epidemic began there. The virus existed in the Kinshasa region by 1959 and began to take epidemic form there by the mid 1970s, perhaps as a result of the wide sexual networks and decayed socio-economic conditions of the city. For nearly ten years, and perhaps more, it remained a silent and unrecognised epidemic. During that period, subgroups of the virus were carried away from the epicentre to infect eastern, southern, and western Africa. Their impact on each region was shaped by its patterns of communications and mobility, its gender relationships and sexual networks, its disease environment and socio-economic arrangements. But in this first HIV/Aids epidemic, the virus initially established itself silently within the general heterosexual population before any steps were or could have been taken to check it. Africa had the worst epidemic because it had the first epidemic.
Second, this silent expansion was one way in which the unique character of the virus - mildly infectious, slow-acting, incurable, fatal - decisively shaped the epidemic and human responses to it. Those responses were slow, for HIV's long, asymptomatic incubation period and the eventual appearance of diverse opportunistic infections defied prompt action and fostered uncertainty and denial. Instead, people with Aids faced a slow and painful death while their families undertook a heavy burden of care and mourning. Care and death impoverished households and multiplied the orphans to whom young adults gave birth before they died. Yet slow incubation also gave people with HIV/Aids time to organise themselves for mutual aid and political action.
The third perspective has been to set the epidemic in the longer context of African history. When compared with earlier epidemics, HIV/Aids stands out chiefly by its uniqueness: more enduring than influenza, less environmentally dependent than sleeping sickness, more fatal than tuberculosis.
During the late 1990s and early 2000s response to HIV/Aids was revitalised at both the global and the African levels. Leadership passed from the WHO to the Joint United Nations Programme on Aids (UNAIDS) in 1996, but the main dynamic came from the discovery of antiretroviral drugs (ARVs) that could suppress, but not cure, the disease. ARVs brought hope, the crucial quality needed to activate health workers and people with HIV/Aids. As with previous African diseases, it needed such a magic bullet - penicillin for syphilis, dapsone for leprosy - to stimulate a mass treatment campaign. Yet to make ARVs available to millions of infected Africans required radical changes of attitude among international donors, shifts of power in the pharmaceutical industry, and infusions of energy into African regimes - infusions that might in turn require pressure by those in desperate need of drugs. Here the source of HIV's power - its slow action and long incubation - became its weakness, for unlike many other epidemic diseases it gave infected people time to organise a counter-attack. By 2005 only a small minority of Africans needing ARVs were receiving them and it was increasingly obvious that the drugs, while immensely valuable to individuals, could not reverse the epidemic. The search for a vaccine, which in principle could achieve that goal, was still desperately slow. Nevertheless, between 1996 and 2005 the scene was transformed. Hitherto the virus had held the initiative. Now the victims were taking it.
UNAIDS took responsibility for coordinating international action against the epidemic in January 1996. It grew out of the impatience with WHO displayed by richer, more interventionist international agencies from the early 1990s as they developed separate and often competing Aids programmes. Only the United Nations, it was realised, could bring these agencies together, and even then there was doubt until 1994 whether the World Bank would join the coalition. Based alongside the WHO at Geneva, UNAIDS did not take over its medical functions or those of other agencies, nor was it a funding body. Rather, it sought to coordinate, define, and publicise policies, acting through ‘theme groups’ in each country bringing together the local representatives of the various international agencies.
The HIV-1 epidemic that Kapita Bila had first glimpsed in Kinshasa in the mid-1970s had taken almost exactly ten years to spread and become visible among the African peoples at the three corners of the continent, appearing in Ethiopia, South Africa, and Senegal almost simultaneously in the mid-1980s. Having traced that expansion, it is time to return to President Mbeki's question: why has Africa had the world's most terrible HIV/Aids epidemic? An answer must bring together the nature of the virus, the historical sequence of its global expansion, and the circumstances into which it spread, giving particular weight among those circumstances to gender inequalities, sexual behaviour, and impoverishment. Many existing answers perhaps concentrate too exclusively on the circumstances, arguing for the primary importance of either sexual behaviour or poverty.
The distinctive features of HIV as a virus were that it was relatively difficult to transmit, it killed almost all those it infected (unless kept alive by antiretroviral drugs), it killed them slowly after a long incubation period, it remained infectious throughout its course, it showed few symptoms until its later stages, and when symptoms appeared they were often those common to the local disease environment. This unique combination of features gave a unique character to the epidemic, ‘a catastrophe in slow motion’ spreading silently for many years before anyone recognised its existence. One consequence was that whatever part of the world had the first such epidemic would suffer especially severely, for the epidemic would have time to establish itself, unseen, not only in many people over a large area but in the general heterosexual population, where it would be vastly more difficult to contain than in some limited high-risk group contracting the disease through the initial infection of individuals whose distinctive behaviour patterns had brought them into contact with it.
Thus the fundamental reason why Africa had the worst Aids epidemic was because it had the first Aids epidemic. Understandably, many Africans were initially unwilling to accept this, rejecting the notion that HIV evolved from SIV within Africa, despite the powerful evidence for it, because they felt that it was a racial slur - as indeed some commentators intended it to be.
Eastern Africa was probably the first region to which HIV was carried from its western equatorial origin, along several different routes that cannot now be traced in detail. The virus entered a region divided historically into two contrasting natural and social environments: the well-watered, densely peopled kingdoms around Lake Victoria and on the Ethiopian plateau, and the less centralised societies in the drier savanna country where population clustered only on highland outcrops, in colonial cities along transport routes, and on the Indian Ocean coast. This framework gave HIV/Aids in eastern Africa its distinctive contrast between explosive epidemics in the Lake Victoria basin and the capital cities, on the one hand, and slow penetration into the remainder of the region, on the other. Varying relationships between cities and countryside were especially important in the process, as were the mobile groups linking them together and the factors - widespread labour migration, male predominance in urban populations, low status of women, lack of circumcision, and prevalence of sexually transmitted diseases - that bred higher levels of infection than in western equatorial Africa.
The virus first entered the Lake Victoria basin bordering the DR Congo. Patients from Rwanda and Burundi were seen alongside Congolese in European hospitals during the late 1970s and early 1980s. They not only led expatriate researchers to visit Kigali as well as Kinshasa in 1983 but encouraged observers of the epidemic to believe that Rwanda, Burundi, and perhaps even Uganda had been simultaneous or even earlier places of origin alongside western equatorial Africa. The location of the chimpanzee host makes this unlikely, however, as does the distribution of HIV-1 subtypes, for there is no indication in the Lake Victoria basin of the diversity of strains found in the DR Congo. Until well into the epidemic, the A and D subtypes dominated the region.
In Rwanda the first probable case recorded was a mother who displayed characteristic opportunistic infections in 1977 and subsequently tested positive for HIV along with her husband and three children. A retrospective study found that by 1982 some 12 per cent of blood donors in Kigali were infected.
I am indebted to the staff of many libraries: University Library, Medical Library, African Studies Centre Library, and St John's College Library, Cambridge; London School of Hygiene and Tropical Medicine; School of Oriental and African Studies, London; British Library for Development Studies, Falmer; British Library, London and Boston Spa; Library of Congress, Washington; South African National Library, Pretoria and Cape Town; University of Cape Town Library; Cullen Library, University of the Witwatersrand; Ministry of Health, Entebbe; Makerere University Library; Albert Cook Memorial Library, Kampala; Medical Library, Kenyatta National Hospital, Nairobi; and Medical Library, Muhimbili Medical Centre, Dares Salaam.
Among individuals I am especially grateful to Shane Doyle, Pieter Fourie, John Lonsdale, Margie Struthers, David Throup, and Megan Vaughan. James Currey Publishers deserve my thanks for the urgency with which they have undertaken publication.
Writing the book has left me with profound respect for the epidemiologists and medical scientists on whose work it draws. If, through ignorance or hubris, I have misrepresented any of their findings, I apologise in advance.
Just as the nature of the immunodeficiency virus chiefly determined its pattern of expansion, so it also compelled societies to erect particular kinds of defences. Whereas easily transmitted and rapidly fatal diseases like the ‘three-day flu’ of 1918 had demanded brief, urgent, and predominantly medical responses, the years of incubation and months of terminal decline characteristic of HIV created an overwhelming need for long-term care. African governments, impoverished by economic depression and structural adjustment, could not provide this. Instead, late twentieth-century culture offered another model: the non-governmental organisations already active both in global relief work and in many smaller welfare functions in African countries. Along with government bodies, NGOs were largely responsible for preventive work and the support of HIV-positive people during the incubation stage. Initially they also attempted to care for those sick with Aids, but the numbers quickly overwhelmed them and instead this burden fell chiefly on the patients’ families. It was a cruel burden, for in their final months of illness people with Aids needed much intimate and distressing care. Family responses varied, but predominantly they - and ‘they’ meant chiefly women - provided care with a selflessness that was one of the most heroic features of the epidemic. This was not unique to Africa: Aids epidemics everywhere evoked remarkable displays of compassion. What was unique to Africa was the scale of the response in a continent where HIV/Aids was, in this as in other senses, a family disease. Had Africa's family systems been less resilient, the impact of the first Aids epidemic could have been terrible beyond imagining.
The scale and diversity of NGO action defy summary. In 1992 Uganda already had over 600 NGOs involved in Aids work; by 2003 there were about 2,000. Kisumu, the provincial capital of Kenya's heavily infected Nyanza province, had over 200 NGOs and community-based organisations combating Aids in 1999. Senegal was also rich in organisations, over 700 receiving public subsidies during 2004, the same number as those affiliated to Nigeria's Aids programme. South Africa had a vigorous NGO tradition, inherited especially from the anti-Apartheid movement, and counted over 700 bodies engaged in Aids work as early as 1993.
The chief reasons for the failure of international Aids policies in Africa during the late twentieth century were that they came too late to check an expanding epidemic and had no effective medical remedy with which to do so, but another reason was that the medical thinking underlying international policies often conflicted with the ways in which most Africans perceived the crisis. Their responses were diverse, as is commonly true in epidemics, but this was particularly so with HIV because its long incubation period and lack of distinctive symptoms bred confusion and encouraged denial. At an individual level, as a Ugandan woman said, ‘Everybody suffers from silimu differently.’ At the collective level, understandings were set within the context of a long dialogue between indigenous notions of causation, which were chiefly moralistic, and the medical explanations propagated by governments and Western-trained doctors. Similar debates surrounding cholera epidemics in nineteenth-century Europe and America had resulted in victory for medical explanations because they worked, but in late twentieth-century Africa the doctors had no effective remedy and moralism remained powerful. Yet this moralism was not merely traditionalist, for it had blended with the imported moralism of world religions. The result was a hybrid, a popular response to the epidemic that was at once stigmatising, caring, and capable of motivating behavioural change.
The initial response to HIV/Aids was commonly to blame Others. Indignant at suggestions that the virus had originated in Africa, intellectuals insisted that it was rather ‘the white man's burden’, a disease of American and European homosexuals, imported, it was said in Kinshasa, in canned food threatening both health and authenticity. Villagers in Burkina held that HIV originated when a white man paid a woman to have sex with a chimpanzee. The ANC's periodical suspected ‘the laboratories of many imperialist countries’. Other black South Africans saw it as an Apartheid device, spread perhaps by teargas, designed to decimate the black population - an outcome described by one white extremist as ‘like Father Christmas’. Immigrants and refugees from other African countries were widely held responsible. Villagers blamed townsmen. Elders blamed the young. Men and women blamed one another.
HIV-1 first became epidemic during the 1970s in western equatorial Africa, its place of origin. It was at first a silent epidemic, unnoticed until established too firmly to be stopped. In this region, also, during the mid 1980s, the epidemiology of heterosexual HIV/Aids was first determined, exposing a pattern whose main features were to extend throughout sub-Saharan Africa but whose local peculiarities were also to limit epidemic growth within the western equatorial region itself. From this region, moreover, variants of the virus were carried to the rest of the continent.
Although HIV-1 had almost certainly existed in western equatorial Africa since at least the 1950s, it had hitherto struggled even to survive in a sparsely populated region of difficult, often forested environments and poor communications. This was clear from a group of villages at Yambuku in the north of the DR Congo. Blood taken from 659 villagers there in 1976, during one of the first outbreaks of Ebola virus, later revealed that five (0.8 per cent) were infected with HIV. When the villagers were tested again ten years later, HIV prevalence was still 0.8 per cent. Of blood samples collected across the border in southern Sudan in 1976, 0.9 per cent subsequently revealed HIV. Such low levels of infection may well have existed in other rural areas of the equatorial region during the 1970s. They apparently existed also in Kinshasa. One of those testing positive at Yambuku had probably contracted the disease in the capital during the early 1970s. Of 805 blood specimens taken from pregnant women in Kinshasa in 1970, two later revealed HIV infection. So did blood taken there in 1972 from two of four patients with Kaposi's sarcoma.
The conversion of this low-level infection into an expansive epidemic probably took place in the urban environment of Kinshasa during the 1970s. The key may well have been the exceptional infectivity of the newly infected, which meant that if the virus entered a network of sexual relationships in which partners were exchanged rapidly and extensively, it could build up a momentum of infection sufficient to reach epidemic levels.
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'lvoire, 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'lvoire, 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. 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'lvoire, while group B was found chiefly in Côte d'lvoire and Ghana, although scattered cases of both existed elsewhere. 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. 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.
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