Among the original sixty-six AIDS diagnoses of Haitians living either in the eastern United States or Port-au-Prince, only nine definitely fell ill prior to 1981; eight in 1980 and one in 1979.158
According to one theory explaining Haiti’s relatively high early incidence of AIDS, the country was the unfortunate recipient of the U.S. epidemic, carried there by vacationing gay men who hired local male prostitutes. An opposing argument suggested that the gay epidemic may have originated in Haiti. Again, the putative connection was male prostitution and wealthier North American gay vacationers.159
There were then two proffered explanations for HIV’s prior presence in Haiti. The first, espoused by Robert Gallo and Harvard’s Kennedy School of Government public health professor Yamil Khouri, saw a connection between Zaire and Haiti. Zaire imported nearly 10,000 Haitians a year for short-term contract work between 1960 and 1975. Under the Gallo/Khouri theory, HIV already existed in Zaire at that time, and was carried back to Haiti by returning contract workers.160
Always on Peter Piot’s mind when he contemplated the origins of the global epidemic was that Greek fisherman he had treated for AIDS in 1978. When the ELISA test became available, Piot tested the fisherman’s blood, confirming that the man who had spent most of his adulthood fishing in Zaire’s Lake Tanganyika had, indeed, died of AIDS.
By 1984 Piot and other researchers had determined that 3 to 4 percent of the women who gave birth in Kinshasa hospitals in 1980 carried antibodies to the virus, but none of Nairobi’s pregnant women was infected until 1982. By 1984 the infection rate among them was still only 2 percent, Piot said, arguing that “AIDS arrived in Kenya around ’82 or ’81. In any case, later than in Central Africa.â€
Between 1981 and 1984 infection rates among Nairobi’s poorest prostitutes soared from about 4 percent to over 59 percent, lending further credence to assumptions that Kenya’s epidemic was a new, still exploding one. The highest Kenyan infection rates were among recently immigrated Ugandan and Tanzanian prostitutes.161
Evidence from countries peripheral to the equatorial center of Africa—Zimbabwe, Zambia, Mozambique, southern Tanzania—paralleled Kenya’s: AIDS appeared to have radiated outward from the Lake Victoria region, reaching adjacent areas sometime after 1980.162
For example, Dr. Jeff Luande, head of Tanzania’s Tumorcentre, located in Dar es Salaam, closely followed Kaposi’s sarcoma cases in his country. Working back in time through medical records, Luande said, it was apparent that changes began taking place among the country’s cancer patients sometime in 1982. Patients from the country’s north, particularly Bukoba, began to appear for cancer treatment that was complicated by numerous infectious diseases, particularly the previously rare Pneumocystis pneumonia.
Luande, who had received his medical training at Harvard, had a great deal of experience with cancer treatment, and it was a certainty, he said, that the type of Kaposi’s sarcoma he began to see in 1980, first in a trickle and later in torrents, was different from the endemic African form of the skin cancer. The traditional KS, he said, presented with hard, round nodules on the skin of the arms and legs that would enlarge and darken over a period of years. It was undoubtedly a surface skin disease, slow to become malignant, relatively easy to control.
But the new type of KS spread very rapidly and instead of hard nodules, the AIDS KS was splotchy, lighter in color, comparatively soft, and painless to the patients. The lesions were rarely round; rather, they were “spindly,†he said. And AIDS KS tumors could be found all over the body—not just on the arms and legs. Luande was particularly intrigued to find so many patients with KS lesions around lymph nodes. This type of Kaposi’s sarcoma, he insisted, “is a different, new disease.â€
Similar shifts in Kaposi’s sarcoma were seen elsewhere in Africa. In Kinshasa, the numbers of KS cancers tripled between 1970 and 1984. And the case reports of the new, aggressive type of KS leapt eightfold in 1981 alone. Zambia and Uganda also reported startling jumps in the numbers of aggressive KS cases during 1982.163
Based on seroepidemiology—the evidence obtained from blood tests—the highest African infection rates prior to 1984 seemed to have centered on the equator, with latitude ranges of about five degrees northward and ten degrees to the south. Longitudinally the epicenter seemed to range from 15 to 35 degrees. The geographic area, then, encompassed a largely tropical region that included parts of Angola, Zaire, Uganda, Rwanda, Burundi, Tanzania, and Zambia.
The highest infection rates in the region were among female prostitutes, in greatest measure involving women originally from the eastern Lake Victoria region.
Summarizing these findings in a speech before the Second International Conference on AIDS in Paris in 1986, Zaire’s Kapita said, “Something dramatic happened in 1975.†Prior to that year aggressive Kaposi’s sarcoma cases were so rare as to be considered exotic; beginning in 1975, however, the numbers of aggressive KS cases diagnosed in Kinshasa doubled every year. Prior to 1975 cytomegalovirus infections were also rare in Zaire: afterward, they, too, increased dramatically every year, Kapita said.
Kapita could not explain these events. He could only reiterate that “something happened in 1975.â€
San Francisco’s Jay Levy, working in collaboration with Italian and other U.S. scientists, tested a variety of different blood and tissue samples collected in Central Africa between 1964 and 1975, finding no evidence of HIV infection. The samples came from Tunisia, Algeria, Uganda, Zaire, Cameroon, and Senegal.
“Our data, as well as epidemiologic studies in Africa, suggest that the AIDS virus was not prevalent and did not spread in that continent until recently,†Levy’s group concluded. “Thus, HIV appears to have emerged in Africa about the same time as in the United States.â€164
If human factors were the key to the emergence of HIV, there were obvious events in the United States and Europe that could have contributed to sudden viral spread in or around 1975: the gay bathhouse scene, a rapid increase in injecting drug activities, the international expansion of the blood products industry. Less clear were which social factors might have played a role at that time in Central Africa.
The period 1970–75 was marked by guerrilla warfare, civil war, tribal conflicts, mass refugee migrations, and striking dictatorial atrocities in some parts of Central and Southern Africa. Such strife could have affected the historic course of HIV in both direct and indirect ways. Most African military conflict was low-intensity: the weaponry and the strategies were more typical of protracted guerrilla operations than of the Northern Hemisphere’s conventional or nuclear warfare. Rather, opposing forces sought to simultaneously cripple one another economically, politically, socially, spiritually, and militarily, often claiming horrendous numbers of civilian lives.
In protracted low-intensity warfare the deeds of war could not be carried out anonymously. The enemy had faces. Soldiers seized villages and imposed their rule on civilians. Brutality and rape easily became companions to more legitimate forms of combat.
The net results were several human activities that were advantageous for sexually transmitted microbes: increased multiple partner sexual behavior (whether voluntary or not), famine or malnutrition that stressed immune systems, large-scale migrations of people from remote areas to central zones of food supplies or safety, increased prostitution, and diminution or devastation of health care services.165
During 1970–75 sub-Saharan Africa was the victim of so much strife that it would be difficult for scientists to pinpoint a “worst case†event that could be blamed for the sudden scourge of HIV. It was, for the continent, a time of tremendous instability. The former Portuguese colonies (Angola, Mozambique, Cape Verde, Guinea-Bissau) were given self-rule only in 1975; civil war and revolution raged across Africa’s southern belt (South Africa, Namibia, Ang
ola, Mozambique, Zimbabwe); and dangerous despots exerted brutal rule over several nations, and manipulated ethnic conflict, noticeably in the Central African Republic, Uganda, and Zaire. Finally, the entire region was locked in conflict with the only economically powerful nation on the continent, the apartheid state of South Africa.
Uganda’s crisis was probably the most acute. Idi Amin’s ruthless rule was unchallenged and absolute during the early 1970s and the concomitant massive social and economic disruption is well documented. Over 45,000 Asians were expelled from the country, tens of thousands of black Ugandans sought refuge in neighboring countries, virtually all foreign investors and professionals fled, and Amin, hungry for expanded territorial control in Africa, spent the country into bankruptcy purchasing arms on the world’s open market.
As the Amin government printed ever more currency, the official economy became worthless, and the marketing hubs shifted from the old urban centers to remote areas that were conducive to smuggling. Tiny Lake Victoria fishing villages were transformed overnight into busy smuggling ports. As a business, prostitution was second only to the black market.166 For most women there were only two choices in life: have babies and grow food without assistance from men, livestock, or machinery, or exchange sex for money at black-market rates.
Nowhere was the situation more acute than in the Rakai District, along the Tanzanian border. The area became a vast lattice of mud roads, brothels, and smuggling centers through which flowed a steady stream of truckers carrying cargoes bound for Kenya, Tanzania, Rwanda, Burundi, and Zaire.
The 1979 overthrow of Amin would only continue the crisis, putting it in the hands of President Milton Obote. Famine would strike, particularly in the West Nile region of northern Uganda. An estimated 300,000 had already fled that area as refugees from Amin’s brutality. They had taken up unwelcome residence in eastern Zaire, Uganda’s Rakai District, and southern Sudan. As famine conditions worsened, the refugee flow would turn into a tidal wave, and the 1983 census would reveal that 57 percent of the region’s former residents were either dead or living elsewhere.
The famine would expand in 1982 into southern Uganda—particularly the Rakai and Mbarara districts—and ethnic tensions would become violent. Clashes between local residents and the tens of thousands of refugees in the area (who came not only from northern Uganda but also from Rwanda, fleeing political massacres), would drive even the black-market economy into chaos.
Nearly all of Africa’s social and political upheavals had multilateral ramifications, and several served as proxy Cold War confrontations between the United States and the Soviet Union. The region’s governments and insurgents were armed to the teeth, and even local tribal warfare became increasingly high-tech and costly in human lives as the decade wore on. The civilian toll, both in direct loss of life and in social disruption, home-lessness, famine, and refugee migration, was severe.167
Sorting out which, if any, of these upheavals might have played a role in the emergence of Africa’s AIDS epidemic seemed a daunting task. In addition to such obvious dramatic events there were the long-term and escalating phenomena of rapid population growth, even more rapid urbanization, and tremendous poverty.
McCormick considered the problem of deciphering what, if anything, happened from the point of view of HIV in 1975, and decided that the easiest first step would be to pull those old vials of blood from the Yambuku and N’zara epidemics out of the CDC’s deep freeze and test them for HIV antibodies.
He discovered that 0.8 percent (5 of 659) of the blood samples collected around Yambuku in 1976 were infected with HIV. The infected individuals ranged in age from nine to fifty years; three were female, two male. Similarly, just under 1 percent of the serum samples he had collected in southern Sudan in 1979 had antibodies to HIV.168 McCormick selected Belgian-born CDC epidemiologist Dr. Kevin De Cock to do the fieldwork, and in early 1985 De Cock made a difficult journey to Yambuku, this time in search not of Ebola but of HIV.
His task was to find the five individuals who had tested positive in 1976 and take fresh blood samples. He also wanted to gather a representative blood sampling of the area for general HIV analysis at the CDC.
De Cock found the local Zairois fed up with all the poking and testing, the unpleasantness of being studied by dozens of foreigners nine years earlier still fresh in the collective memory. There was a haunted, eerie feeling to the place, which still reeled from the terrible, frightening plague of 1976. De Cock was led to graveyards, shown the rows of those family members who were buried one after another as Ebola swept over the population. And every adult spoke on a time scale in which all the world’s history was “before Ebola†and events since the fall of 1976 were “after the virus.â€
He found two of the individuals who had tested HIV-positive in 1976. A middle-aged man and woman were healthy, still tested HIV-positive, and the woman’s T-cell count seemed normal. The man had an abnormally low T-cell count.
The other three 1976 HIV-positive individuals had died, all victims of an ailment that could have been AIDS. One of the dead was a woman who lived in Kinshasa from 1972 to 1976 as a “free woman,†returning to Yambuku shortly before the Ebola epidemic began. “Free woman,†or femme libre, was a Zairian euphemism for prostitute.
The overall prevalence of HIV-positive individuals in the Yambuku area in 1985 was the same as in 1976: just under 1 percent.169 Though the virus was present, there had never been a Yambuku AIDS epidemic.
As McCormick, De Cock, and Zairian colleague Nzila analyzed the data, they reached a set of conclusions: HIV had been present in remote regions of Central Africa for a long time, infecting small numbers of people. The social customs of traditional village life limited the spread of HIV and other sexually transmitted diseases, they argued, as extramarital and premarital trysts were condemned and virtually impossible to conceal in the claustrophobic atmosphere of the tiny communities scattered throughout equatorial Africa.
“The stability of HIV infection in rural Zaire over a long period contrasts sharply with the epidemic spread of the virus in major African cities,†they wrote. “Our findings suggest that the traditional village life in the Equateur province carries a low risk of HIV infection. The disruption of traditional life styles and the social and behavioral changes that accompany urbanization may be important factors in the spread of AIDS in Central Africa.â€
To bolster their conclusion that urbanization and its concomitant erosion of traditional sexual taboos and lifestyles was key to the emergence of HIV in Africa, the CDC and Project SIDA scientists devised a unique experiment: they took blood samples from people living and working along the Congo River, Zaire’s equivalent of a superhighway for shipment of goods and travelers. In this way they hoped to track the social pattern of the spread of the virus.
They found a clear pattern of HIV dispersal radiating from river inns, where the male boat workers and traveling salesmen would spend their nights in the company of prostitutes. In the far eastern section of the river, just below the Yambuku area, very few riverside residents, including prostitutes, were infected. But as they progressed southwesterly along the Congo River, drawing ever closer to Kinshasa, the incidence of HIV infection rose steadily among the femmes libres, boatmen, salesmen, and local residents. The highest rates of infection were near the river’s end, inside Kinshasa.
“In many ways an urban center may be considered an ecosystem that can amplify infectious diseases,†they concluded.170 “This appears to have happened with HIV in various African cities. The conclusion we draw from our study is that AIDS in Central Africa has spread not simply because the virus is present, since in one remote area that prevalence of HIV infection has remained low for over a period of 10 years. A change in the interaction between the agent, the host, and the environment is usually required for an epidemic to develop. In this context, we believe that s
ocial change, including the effects of urbanization and population movements, merits consideration in our attempt to understand the changing patterns of disease.â€
Understanding how human activities were related to the presence and spread of HIV in Central Africa before 1981 still didn’t answer questions about when and where the virus first emerged. The 1959 Manchester case argued for HIV’s presence somewhere along the sailor’s voyages around the planet, going back nearly three decades. But how long had it been in Africa?
Max Essex’s group at Harvard, together with scientific teams from Emory University in Atlanta, Duke University in North Carolina, and the University of Washington in Seattle, tested 1,213 plasma samples collected between 1959 and 1982 in Zaire, Congo, South Africa, and Mozambique: one 1959 sample repeatedly tested positive for antibodies to HIV. It came from an individual (gender not known) who resided in colonial Leopoldville in 1959. Leopoldville was renamed Kinshasa when Patrice Lumumba took power; the 1959 sample was designated the “Leopoldville strain.â€171
The debate about where and when the human immunodeficiency virus emerged was radically affected by two other discoveries: that Old World monkeys carried HIV-like viruses, but New World simians did not; and that there was a second species of AIDS virus, dubbed HIV-2, which seemed to exist only in Africa.
The Coming Plague Page 57