Читать книгу The African AIDS Epidemic - John Iliffe - Страница 11

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Epidemic in Western Equatorial Africa

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.¹ 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.²

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. That is probably what happened in the United States, where HIV prevalence among homosexual men attending a sexually transmitted disease clinic in San Francisco rose between 1978 and 1984 from 1 per cent to 65 per cent.³ It happened at much the same period, although less explosively, among heterosexuals in the East African cities of Bujumbura, Kigali, and Nairobi, as also in rural south-western Uganda and in Abidjan in West Africa. The first occasion, however, was in Kinshasa, where HIV first encountered rapid partner exchange in urban sexual networks wider, although not necessarily much more promiscuous, than those of the countryside.

Map 1 Western Equatorial Africa

The first person to notice the change may well have been Dr Kapita Bila, the Congolese physician heading the internal medicine department at Kinshasa’s huge, 2,000-bed Mama Yemo Hospital. ‘Something dramatic happened in 1975,’ he recalled a decade later, referring especially to a doubling of cases of Kaposi’s sarcoma, a tumour that could take aggressive forms when the immune system was damaged and hence often became a conspicuous symptom of Aids. Other hospitals in the region observed this increase only in the later 1970s and early 1980s, but Kapita Bila dated it at Mama Yemo from 1975 and claimed that hospital records revealed cases at that time. The records also confirmed Congolese doctors’ recollections that in the mid 1970s they had first noticed numerous cases of the severe wasting and diarrhoea that became the most common symptoms of Aids in African patients.⁴ In the late 1970s doctors across the river in Brazzaville observed similar cases. Physicians in Kinshasa initially attributed these symptoms to tuberculosis, which spread epidemically in the region during the 1970s and 1980s, perhaps in synergy with HIV. By 1985, one-third of tuberculosis patients in Kinshasa’s hospitals also had HIV.⁵ A more distinctive indicator of Kinshasa’s emerging HIV epidemic was cryptococcal meningitis, an agonising and commonly fatal infection of the brain. Hitherto generally confined to children, it spread in a distinctively urban form to adults with damaged immune systems and became increasingly common at Mama Yemo from the late 1970s.⁶

When blood taken in 1980–1 from antenatal clinic attenders in Kinshasa was later tested, it showed that HIV prevalence among them had grown during the 1970s from 0.2 per cent to 3 per cent.⁷ The world’s first HIV epidemic among a heterosexual population had begun before the existence of the virus was even suspected. That, more than anything else, was why Africa was to suffer so terribly during the following decades. Yet enlightenment now came quickly. In June 1981 American doctors published the first account of an epidemic of pneumocystis carinii pneumonia among American homosexuals. On reading it, physicians in Brussels and Paris realised that they had treated similar conditions since the mid 1970s, chiefly in Africans from the equatorial region or Europeans who had visited it. Of the first 96 recorded Aids patients seen in Europe, 54 were Africans, 40 of them from the DR Congo.⁸ In contrast to infected Americans, however, they were heterosexuals in roughly equal numbers of men and women, they did not take drugs, and they had no obvious risk factor in common except their geographical origin. In October 1983 joint American and Belgian teams left for Kinshasa and Kigali.

At Mama Yemo, Kapita Bila showed the visitors the patients he suspected to be suffering from Aids. ‘The moment I walked into the hospital in Kinshasa I realised something terrible was happening,’ recalled Peter Piot, later the first head of UNAIDS.⁹ ‘Meningitis was only one manifestation of the disease,’ wrote his colleague Joseph McCormick:

Some developed such exquisitely sore mouths and tongues that they were unable to eat. Those who could manage a few bites of food were suddenly stricken by cramps and disgorged a copious amount of diarrhea. Their skin would break out in massive, generalised eruptions. Infected fungating masses would appear inside and outside their bodies. When the infection didn’t consist of voracious yeast cells [as in cryptococcal meningitis], there were many other parasites ready to eat the brain alive. None of the victims could comprehend in any way what was happening to them or why. And we? All we could do was watch in horror, our roles as physicians reduced to scrupulous observers and accurate recorders of documentation. Our one hope was that if we could understand the processes we were observing, someone, somewhere, might find some solution.¹⁰

Diagnosing by symptoms, the team identified 38 Aids cases in Kinshasa’s hospitals, 20 men and 18 women. Of these, 29 were from Kinshasa itself, but others came from all parts of the country, indicating how far the virus had spread. On 3 November the team presented its findings at a medical meeting at Mama Yemo, warning that the disease appeared to be sexually transmitted, incurable, and fatal. ‘If there is a misfortune spreading terror in Kinshasa in the last few days, it is assuredly AIDS,’ a local editor wrote five days later. ‘It is spoken of in the most varied ways . . . at the office, at the market, in bars, in families . . . Never in my memory as a journalist have I seen such concentration on a subject as disagreeable as strongly feared.’¹¹ It was his last such comment, for President Mobutu’s increasingly unpopular and insecure government banned the subject for the next four years. ‘For the four million Kinois,’ a foreign journalist wrote in 1986, ‘the disease, for lack of any official information, still has no name. Signs, therefore, suspicions, often infantile beliefs. Aids all the same.’¹²

Reactions abroad to evidence that the disease was widespread in a heterosexual population were equally hostile. American medical journals rejected Piot’s report and it took over a year to convince the American government. In the meantime the World Health Organisation cautiously endorsed the discovery by French scientists that Aids was caused by a retrovirus. McCormick persuaded the Centers for Disease Control in Atlanta to fund a research project in Kinshasa.¹³

Projet Sida, as it became known, began work in June 1984 and defined the epidemiology of the urban disease in a form that still dominated medical thought two decades later. A collaboration between American, Congolese, and Belgian specialists, initially led by an idealistic public health expert named Jonathan Mann, the Project had nearly 300 staff at its peak and the advantage of newly devised equipment to test blood for HIV. Its most important finding was that between 6 and 7 per cent of pregnant women at Kinshasa’s antenatal clinics were already infected with HIV, whereas earlier estimates of the epidemic had observed only the much smaller numbers with advanced Aids. Mann warned in 1986 that ‘one to several million Africans may already be infected’. He reckoned the annual incidence of new infections at between 0.5 and 1.5 per cent of hitherto uninfected people.¹⁴ The Project also identified the means of transmission as sexual intercourse, exchange of blood by injection or transfusion, and infection from mother to child, excluding aerial transmission, insect vectors, and casual contact.¹⁵ Sexual transmission was bidirectional, whereas the possibility of women infecting men had hitherto been uncertain. Among new infections, eleven were women to every ten men, although women in their twenties outnumbered men by three to one.¹⁶ In other respects those infected did not have a strong social profile. The earliest observed cases had often been prosperous people who could afford multiple partners and medical treatment, but antenatal prevalence at Mama Yemo was somewhat higher than at a fee-paying hospital. The age profile, however, was distinctively bimodal, peaking in infants and young adults.¹⁷ Perinatal transmission and pediatric Aids were among the Project’s most novel findings. Mothers with HIV lost 24 per cent more of their babies in the first year of life than did those without it, the risk varying with the stage of the mother’s disease.¹⁸ Adult HIV was associated with tuberculosis and sexually transmitted diseases, the latter being one of several indications linking HIV to risky sexual behaviour. Some 27 per cent of Kinshasa’s commercial sex workers had HIV.¹⁹

The Project also revealed an alarming connection between HIV transmission and blood transfusion, which had become common in large African hospitals since the Second World War. Mama Yemo gave about 80 transfusions a day, chiefly in childbirth or to severely anaemic children. The blood came from relatives or was bought from unemployed people recruited at the hospital gates. At least 5 per cent was infected with HIV. Since transfusion almost invariably transmitted the virus, the hospital was creating four new HIV cases each day. Of its patients aged 2–14 and too old to have been clearly infected perinatally, 11 per cent were HIV-positive and 60 per cent of these had received transfusions.²⁰ Injections with re-used and unhygienic needles were another alarming danger, for injections had been immensely popular among African patients since the 1920s. The Project found that one group of HIV-infected children under 24 months old with HIV-negative mothers had received an average of 44 injections (excluding vaccinations) during their lives. Among adults, HIV prevalence increased with the number of injections received. It was impossible to demonstrate causation, for patients may have needed injections because they were already ill, but Mann concluded that infected blood was a significant factor in HIV transmission, although, as the age profile suggested, sexual intercourse was more important.²¹

Projet Sida effectively ended in 1991 when rioting soldiers looted its premises and the expatriate staff withdrew, although Congolese doctors tried to continue the work. Meanwhile research had also revealed the extent of HIV elsewhere in the western equatorial region. Kinshasa’s epidemic had spread up the river and into the neighbouring Lower Congo area, where estimated adult prevalence reached 4 per cent in semi-urban and 2.8 per cent in rural areas in 1989–90.²² The distant mining towns of Katanga and their surrounding rural areas had similar prevalences at that time,²³ but little was known about the countryside outside the Lower Congo. Kinshasa’s epidemic seems to have made only a limited impact on the immensity of the country at this period. Brazzaville, across the river, appears to have shared Kinshasa’s epidemic pattern at a slower tempo. In the late 1970s it saw symptoms later characteristic of Aids and in 1983 it sent patients to France for positive investigation. The urban epidemic then grew quickly, reaching an adult prevalence of 8 per cent in 1991, while spreading at roughly half that level to Ouesso in the north, Pointe-Noire in the west, and the rural Niari region neighbouring the capital, although expansion into the sparsely-populated countryside elsewhere was slow.²⁴ By contrast, in Gabon, further to the north-west, an epidemic emerged more slowly. The first evidence of HIV there dated from 1983 and antenatal prevalence in the main towns of Libreville and Franceville rose only slowly to less than 2 per cent between 1986 and 1994, with even lower levels in the countryside.²⁵ Cameroun had a different but equally unspectacular experience. Perhaps because it was probably a site of early HIV evolution, the disease there remained scattered, much as it had been in the DR Congo until the later 1970s. Between 1986 and 1988 researchers in Cameroun found only 23 cases distributed among a dozen towns. This excluded the two main cities, Yaoundé and Douala, but neither played Kinshasa’s role in breeding an epidemic. In 1992 each had an antenatal prevalence only slightly over 2 per cent. Instead, Cameroun’s highest HIV concentrations at that time were on its eastern border with the Central African Republic.²⁶

This was because the CAR experienced an epidemic more striking than Kinshasa’s, expanding more rapidly both in the capital and to the rest of the country. Doctors in Bangui began to suspect Aids in 1982, confirmed it late in 1983, and came to think that they had seen it some years earlier in cases of cryptococcosis, tuberculosis, Kaposi’s sarcoma, diarrhoea, and wasting. HIV must certainly have reached the region by the 1970s. Prevalence in Bangui’s general population aged 15–45 rose from 2.3 per cent in 1985 to 7.8 per cent in 1987. By 1993 prevalence among antenatal women there had reached 16 per cent.²⁷ French doctors blamed the epidemic on sexual behaviour in a rapidly expanding town dominated by unmarried young people from a countryside with traditions of considerable sexual freedom. In 1987, 58 per cent of respondents aged 15–44 had had a child before the age of 20, 54 per cent reported extra-marital sex, 81 per cent had suffered a sexually transmitted disease, and only 34 per cent had used a condom. The epidemic was not primarily due to prostitution – not more than 21 per cent of Bangui’s sex workers were HIV-positive during the later 1980s – but to rapid partner change, averaging between 20 and 40 partners a year according to a group of 56 men and 49 women examined in 1983–5, 60 per cent of whom were HIV-positive. Many poor young women engaged in sporadic subsistence sex. Multiple injections – eight a year on average for those with both HIV and tuberculosis in 1985–8 – added to the risk.²⁸

From about 1985, when prevalence began to grow rapidly in Bangui, the epidemic also spread more widely. By 1990 some provincial towns in close communication with the capital had adult prevalence rates of 8 per cent. Two years later similar levels were recorded at Berberati and Gamboula, truck-stop towns near the Cameroun border with ties to diamond diggings that attracted many young people, while at Mbaimboum, where Cameroun, Chad, and the Central African Republic met, the prevalence among women in 1993 was 22.8 per cent. In parts of the DR Congo bordering the CAR Aids was known as ‘Bangui’.²⁹

This account of the epidemic’s origins in western equatorial Africa has indicated distinctive circumstances that both enabled HIV-1 to establish itself as a human epidemic and constrained its growth within the region. Two circumstances were especially important. One was the mobility fostering the rapid spread of disease among young urban immigrants, truck drivers, alluvial miners, and their female partners, although constrained everywhere in the region by distance, insecurity, transport difficulties, and sparsity of population. The other was the rapid urbanisation that had begun in the later colonial period and escalated amidst postcolonial conflicts. Kinshasa had some 400,000 inhabitants when the earliest infected blood was collected there in 1959 and four times as many when indications of an epidemic first appeared in the mid 1970s. Once known as Kin la Belle (Kinshasa the Fair), it had become Kin la Poubelle (Kinshasa the Dustbin). Its decaying modern core was ringed by unserviced squatter settlements. The real value of its official minimum wage fell by 75 per cent during the first sixteen years after independence in 1960. Unemployment exceeded 40 per cent for men in 1980 and was much higher for women, who made up only 4 per cent of the country’s formal urban labour force.³⁰ While the numbers of men and women in the city were roughly equal and nuclear families predominated, only 70 per cent of adult women were married in 1984, while their lack of economic opportunity other than petty trade, together with a formerly polygynous culture in which young unmarried people had much sexual freedom and gifts were a normal part of love-making, led a proportion of young women to depend on sexual relationships with men either for survival or for otherwise unobtainable goods.³¹ Full-time prostitution was probably less important than in some eastern African cities where women did not trade and men heavily outnumbered them. In 1988 Kinshasa’s sex workers averaged only 8.6 clients a week, compared with 35 among lower-class sex workers in Nairobi in 1987. Their 27 per cent HIV infection in 1985, although horrifying, contrasted with 61 per cent in Nairobi. It was estimated in 1988 that to eliminate all prostitution from Kinshasa would reduce HIV transmission by only 25 per cent.³²

The bulk of transmission was rather among a minority of vulnerable individuals in wide networks of ephemeral sexual relationships in which the men were often significantly older and wealthier than the women. In an illuminating contrast with Rwanda that would have applied to the whole western equatorial region, Michel Caraël observed that ‘Kinshasa, with its bars, its precocious, free, and joyous sexuality despite immense poverty, its litany of bureaux (concubines)’ was ‘light years away’ from the ‘austere Catholic town’ of Kigali, where men had extra-marital relations chiefly with sex workers and then infected their wives, so that HIV was most common in the age range 25–35, whereas in Kinshasa the disease was more widespread among older men and younger women.³³ Kinshasa’s sexual pattern raised HIV to epidemic proportions, but not the explosive proportion seen in Kigali. This was reinforced by the fact that over 90 per cent of men in the western equatorial region were circumcised, which probably provided some protection because the foreskin was especially liable to viral penetration, and that sexually transmitted diseases – although closely associated with HIV infection – were relatively rare, including the incurable genital ulcer disease caused by herpes simplex virus 2 (HSV-2) that was spreading throughout the world in synergy with HIV. A later comparison was to show that, thanks chiefly to these two advantages, Yaounde had significantly lower HIV prevalence than Kisumu in Kenya or Ndola in Zambia, despite high levels of extra-marital sex.³⁴

These constraints help to explain the most remarkable feature of the HIV epidemic in western equatorial Africa: its failure to expand during the 1990s beyond the levels of prevalence reached early in the decade, although those levels were often at or above the threshold 3–5 per cent prevalence commonly thought to trigger exponential growth. In Brazzaville city, for example, prevalence at antenatal clinics fell between 1991 and 1996 from 8 to 5 per cent, suggesting, together with a peak prevalence in older age groups (men of 35–49 and women of 25–30), that this early epidemic had reached maturity at a modest prevalence.³⁵ The epidemic in Bangui, similarly, stabilised between 1993 and 1998, although at a level of 16 per cent that could be sustained only by a high incidence of new cases.³⁶ In Gabon and Cameroun, where the epidemic had begun later, there was more growth during the 1990s, but to adult levels below 7 per cent.³⁷ The most striking illustration was the DR Congo, often considered ‘a risk environment par excellence’,³⁸ where, however, the long-predicted epidemic explosion did not happen. In Kinshasa, for example, HIV prevalence among pregnant women declined between 1985–8 and 1992 from 6–7 per cent to 5 per cent and then remained at or below that level for the remainder of the decade.³⁹

Analysts struggled to explain this surprising stability. Some suggested that the HIV strains evolved so early in this region might be less virulent than those elsewhere, but there was no hard evidence to support this. Others thought that poverty might have reduced the rate of sexual partner exchange.⁴⁰ More convincingly, it was pointed out that in Kinshasa, as in Bangui, the epidemic, having begun so early, had reached a stage of maturity at which a stable prevalence concealed a balance between deaths among older groups and a substantial incidence of new infections, chiefly among the young. Between 1986–7 and 1989–90 in Kinshasa, for example, prevalence among pregnant women under 25 nearly doubled, while among older women it fell slightly. The investigators estimated that the annual incidence of new infections in pregnant women aged 20–24 was almost 2 per cent, nearly twice that in the general population. ‘A stable HIV seroprevalence in sentinel surveys,’ they concluded, ‘may be consistent with a dynamic epidemic.’ The city’s sex workers may have had a parallel experience, prevalence stabilising at about 35 per cent while annual incidence was 10 per cent.⁴¹

Both Kinshasa and the rest of DR Congo also enjoyed some protection against an explosive epidemic from the great distances between population concentrations and the difficulty of travel where transport had widely broken down and much violence and insecurity prevailed, these factors together preventing the linking of sexual networks that commonly fostered epidemics. The falsity of the common belief that ‘war creates the perfect conditions for the spread of AIDS’⁴² was also demonstrated at this time in neighbouring Angola, where national antenatal prevalence after nearly 40 years of warfare was found by a survey in 2004 to be only 2.8 per cent, with the lowest figures in central provinces ‘that have been more protected by the effect of war,’ as the Vice-Minister of Health put it.⁴³ By contrast, the two countries registering modest epidemic growth during the 1990s, Gabon and Cameroun, were the most peaceful in the region.

The limited capacity for expansion shown by the western equatorial epidemic during the 1990s had as its counterpart the survival there – perhaps especially in the countryside – of a diversity of HIV subtypes and recombinant forms far greater than anywhere else in the world. A more explosive epidemic might well have swamped this diversity by a single dominant strain more like those created by founder effects elsewhere. Yet it was from this region that the various forms of the virus were carried to the rest of the continent and the world. The most spectacular illustration was the transmission of the circulating recombinant form CRF01_AE from its hearth in the northern DR Congo and the neighbouring Central African Republic, where alone it was common early in the epidemic, to become the major strain of HIV in South-East Asia, although the means of this transmission are unknown.⁴⁴ A less dramatic example was the other major circulating recombinant, CRF02_AG, which provided 60 per cent of HIV-1 strains in Cameroun during the 1990s, especially in the north, and some 54 per cent in Gabon. Its ancestors probably lay in the DR Congo – one of them was a virus collected at Yambuku in 1976 – but CRF02_AG itself was rare in both Congos during the 1990s and appears therefore to have taken shape in the Cameroun-Gabon region, whence it was carried northwards to become the dominant form of the virus throughout West Africa.⁴⁵ By contrast, the subtypes (as distinct from CRFs) of HIV-1 transmitted to other parts of the continent appear to have been carried directly from the DR Congo. Subtype A was the most common form there, especially in the north, and was carried into East Africa, where it shared predominance with subtype D, itself rare elsewhere except in the DR Congo.⁴⁶ Less certainly, subtype C, which came to dominate southern Africa (and Ethiopia), was common only in the south of the DR Congo, whence it may have been carried southwards.⁴⁷ The history of this radiation from the equatorial region is the next issue to consider.