The Pandemic Century

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  The first evidence for this hypothesis had come in 1983 when serum collected from a woman in the obstetrics ward of Mama Yemo Hospital in Kinshasa tested positive for LAV. The findings prompted Montagnier to conduct further tests on archived blood samples from Zaire dating back to 1970, many of which also turned out to be positive for the virus. At the same time, using the ELISA test, Gallo began examining stored blood samples that had been collected by the National Cancer Institute in 1972 and 1973 from schoolchildren in Uganda as part of a study of Burkitt’s Lymphoma. To his astonishment, these showed that two-thirds of the Ugandan children were infected with HTLV-III.

  In 1983 Peter Piot, a Belgian microbiologist who had become concerned about the number of wealthy Zairians presenting with symptoms of immune deficiency at his tropical diseases clinic in Antwerp, decided to investigate the full extent of the problem in Zaire. Focusing on Mama Yemo Hospital, where doctors had first noted AIDS-like wasting symptoms in the late 1970s, he found that during a three-week period scores of patients on the wards were infected with AIDS. Subsequently he was joined by Jonathan Mann, a former CDC epidemiologist who would go on to become director of the WHO Global Program on AIDS, and the pair began gathering further epidemiological data as part of Project SIDA, the first and largest AIDS research project in Africa. By 1986, they had established that AIDS was an escalating problem in Zaire and Rwanda, with up to 18 percent of blood donors and pregnant women infected with HIV. They also noted that the syndrome affected men and women more or less equally, and that most of the men surveyed considered themselves heterosexuals. If this was not enough to dispel the canard that AIDS was a predominantly homosexual disease, researchers went on to report that up to 88 percent of commercial sex workers in Kinshasa and the Rwandan capital Kigali were also infected with the virus, with a similarly high frequency of HIV infections in their clients.

  However, perhaps the best evidence that the virus had been present in Africa for some time came from retrospective tests of stored serum samples collected during the Ebola outbreak in Yambuku in 1976. Of the 659 samples drawn from patients in villages close to the Catholic mission hospital, 0.8 percent tested positive for HIV. But while the shocking symptoms of Ebola and the high mortality rate had immediately attracted the attention of investigators from the CDC and elsewhere, no one had noticed these HIV infections at the time. If evidence were ever needed of HIV’s cunning, this was it. Unlike Ebola, and other animal-origin viruses that are new to humans, HIV does not draw attention to itself by killing its host suddenly or violently. Instead, the virus has evolved a slow-but-sure strategy that enables it to infect human cells and replicate unnoticed. The result is that people parasitized by HIV can live and quietly pass on the virus for ten years or more before showing any signs of illness. Indeed, it was only in 1985–1986 when three of the villagers in Yambuku developed illnesses suggestive of AIDS that scientists thought to screen the local population for HIV. Interestingly, this survey turned up similar levels of HIV infection as a decade earlier, suggesting that, in rural areas of Africa at least, the virus had made little progress in ten years. This would be an important clue to its epidemiology.

  As scientists began screening other collections of archived sera, so other missed alarms came to light, this time in Europeans. One of the most interesting was that of the Danish surgeon Grethe Rask, who had died in Copenhagen in 1977, after suffering a range of AIDS-like opportunistic infections, including PCP. At the time she became ill, in 1974, Rask had been working in Kinshasa, but prior to that, between 1972 and 1975, she had been based in Abumonbazi, a rural hospital sixty miles north of Yambuku. Initial tests in 1985 using an early version of ELISA were negative for HIV, but when the tests were repeated two years later with more sophisticated assays they were positive for the virus. Another case was that of a Norwegian family—father, mother and nine-year-old daughter—all of whom had died of AIDS-like symptoms in 1976. In 1988, retrospective tests showed they all had HIV, and since the daughter had been born in 1967, this suggested the mother had already been infected by that date. Intriguingly, the father had been a sailor who had visited a number of ports in West Africa in the early 1960s, including Nigeria and Cameroon in 1961–1962. The hypothesis was that at one of these ports he may have slept with a prostitute and contracted the virus.

  By the mid-1980s, evidence of similarly early cases of AIDS were also coming to light in Africa. The first HIV-positive specimen was isolated from a Bantu man who had given blood in 1959 in Léopoldville, the old Belgian colonial name for Kinshasa. The blood specimen had lain in a refrigerator for twenty-seven years. At the time, it was not possible to identify to which HIV group the specimen belonged, but in the 1990s it became possible to amplify genetic material using a new technique called polymerase chain reaction (PCR), and in 1998 scientists established that it belonged to the same group responsible for the vast majority of pandemic infections. Then, in 2008, a group of scientists writing in Nature announced they had sequenced HIV from another specimen, also from Léopoldville. This specimen had been taken from the lymph gland of a woman in 1960, after which it had been stored in the pathology department of the University of Kinshasa. Although the material was badly fragmented, using PCR the team, led by Michael Worobey, an evolutionary biologist at the University of Arizona, were able to sequence a few strands of DNA and RNA. After amplifying the genetic material, Worobey then compared the virus to the earlier isolate from Léopoldville and established that it was a closely related subtype. The next stage was to use a molecular clock to calculate how long it would have taken the two viruses to have diverged from one another. This produced a date for the common ancestor virus between 1908 and 1933 (with a median of 1921). Given the uncertainty of molecular clock calculations (RNA does not mutate at the same rate as DNA), these measures should be viewed with a degree of skepticism. However, there is little doubt that HIV was present in Léopoldville by 1959, and, if Worobey’s calculations are correct, very possibly as early as 1921.

  Using the same PCR techniques, scientists have also gone on to study current circulating strains of HIV. To date, these studies have shown that there are two main types of HIV: HIV-1, which is highly transmissible and is responsible for the vast majority of infections worldwide, and HIV-2, which circulates mainly in West Africa and is associated with comparatively low levels of virus in the blood. To complicate the picture further, HIV-1 has been divided into four groups and one of these groups, group M, has been subdivided into ten subtypes. In addition, if individuals are infected with more than one subtype, the subtypes can swap genes and form new recombinant strains. The result is an alphabet soup highly confusing to the layman.

  Nevertheless, today few scientists doubt that AIDS originated in Africa. This is not only because the two oldest isolates of HIV come from Kinshasa, but because nowhere else in the world does the virus show such diversity. HIV evolves only in one direction, from a single model of a virus to an increasingly complex differentiation into subtypes and recombinants, so viral diversity is strong evidence of point of origin. So far, so uncontroversial. But almost everything else about the origins of HIV and its association with AIDS has been contested. For instance, some retrovirus experts, such as Peter Duesberg, a biologist at the University of California, continue to deny that HIV is the cause of AIDS, even though the virus’s etiological role has long been accepted by all competent scientific authorities. Similarly, the British writer and journalist Edward Hooper maintains that AIDS can be traced to mass polio vaccination campaigns conducted in Central Africa in the late 1950s (Hooper argues that the inhabitants of the Belgian Congo, Rwanda, and Burundi were given an oral polio vaccine, known as CHAT, contaminated with a simian immune-deficiency virus as a result of the chimpanzee cells used in the production of the vaccine). Hooper’s thesis is described in exhaustive detail in his 1999 book, The River: A Journey Back to the Source of HIV and AIDS, and on his website, where he continues to wage an increasingly lonely campaign against his scientific critics,
the vast majority of whom consider the weight of evidence against his theory overwhelming. Whether or not Hooper or his critics will ultimately be proved right, one of the consequences of his and Duesberg’s critiques has been to fuel conspiracy theories about the role of medical Science in spreading AIDS and to undermine faith in AZT and other potentially life-saving drug treatments. This is particularly true of South Africa where Thabo Mbeki, who was president from 1999 to 2008 and who had taken advice from Duesberg, refused people access to antiretroviral drugs, thereby resulting in 330,000 unnecessary deaths from AIDS between 2000 and 2005, according to one study. Similarly, there is evidence that Hooper’s vaccine contamination theory may have contributed to the distrust of modern polio vaccines, particularly in countries such as Nigeria, Afghanistan, and Pakistan where suspicions about the vaccines and the motivations of international health workers have fueled resistance to mass immunization campaigns, jeopardizing the WHO’s attempts to eradicate the disease from its last endemic centers.

  Regardless of the truth or otherwise of these theories, no one disputes that both HIV-1 and HIV-2 are descended from simian immune-deficiency viruses (SIVs) that parasitize, respectively, chimpanzees and sootey mangabeys indigenous to Central and West Africa, and which cause simian versions of AIDS. The question is, how did these viruses jump species or “spill over” from monkeys and become widely amplified in human populations?

  A leading spillover mechanism is thought to be the hunting and butchering of monkeys captured in the tropical rain forests of Cameroon, Gabon, and the Congo—the region that is home to Pan troglodytes troglodytes chimpanzees. When hunters are cut or bitten in the course of capturing the monkeys or when the animals are butchered for the table, their viruses can readily be transferred to humans. Both simian foamy virus (SFV) and the Ebola and Marburg viruses have been acquired from monkeys in this way. Serological tests of pygmies and Bantu huntsmen show that many carry antibodies to SIVs, suggesting that exposure is a common occurrence in nature. Furthermore, from analysis of the genomes of HIV-1 and HIV-2, as well as their various groups and subtypes, it is known that modern HIV viruses are more closely related to their nearest ancestral SIVs than they are to one another. This is evidence that the simian progenitors of human HIVs must have jumped to humans several times in the course of their evolution. However, as only one group of HIV-1—the M group—is responsible for 99 percent of HIV-1 infections worldwide, this also suggests that the AIDS pandemic started not because a lot of people were infected directly from chimpanzees, but because a rare case of infection managed to spread and multiply in humans, something that all the other simian-origin infections that came before and after it had not managed to do. Fortunately, as the isolate taken from the Bantu man in Léopoldville in 1959 belongs to the HIV-1 M group, and it is there that the virus shows the greatest genetic diversity, when and where this event occurred is no longer a matter of conjecture. The pandemic strain of HIV must have been up and running in 1959 in Léopoldville or else in a nearby town in the Belgian or French Congo. It is in answering the question of how this happened that the debate gets interesting.

  Broadly speaking, there are two schools of ecological thought. The first is that a combination of bushmeat hunting and economic and social changes driven by colonialism, plus globalization—better road, rail, and plane connections—are sufficient to account for the amplification of the HIV-1 M group in Africa and the subsequent international spread of the virus. The second is that, yes, all those factors are significant but insufficient to explain how this particular group came to be so widely dispersed, first in urban African populations, and later in rural Africa and the rest of the world. This is because, in practice, it is very difficult for a simian virus to establish itself in a new human host. Indeed, many SIVs that cause infection in the short term are rapidly eliminated by the host’s immune response. Even if an infection establishes itself in one person, the virus may not spread easily to others. To explain that we need an additional amplifying effect, and the best candidate is provided by medicine. In particular, Jacques Pepin, the leading proponent of this school, points to the reuse of inadequately sterilized hypodermic needles and syringes in the administration of drugs against venereal diseases such as syphilis and tropical diseases such as malaria and yaws in clinics across Africa. As transmission of HIV-1 is ten times more effective through shared needles and syringes than via sexual intercourse, Pepin, a Canadian infectious disease specialist and epidemiologist with broad African experience, argues that these well-meaning medical interventions, many of which were launched during the colonial era, could have given the virus the boost it needed to go from a localized urban epidemic in Léopoldville/Kinshasa to one capable of infecting people as far away as Haiti, New York, and San Francisco.

  Unfortunately, it is not possible to go back in time and test Pepin’s theory by conducting serological tests of patients who attended clinics in the Congo and elsewhere in the colonial period. The only evidence available is historical serum samples containing surviving fragments of HIV, and inferences from analogous examples of the inadvertent transmission of other blood-borne viruses via needles and syringes used in humanitarian medical programs. A good example of the latter is the tragedy that occurred in Egypt during the government campaigns against schistosomiasis, a potentially fatal disease caused by a parasitic blood fluke spread by snails that live in irrigation channels along the River Nile and other watercourses. Between 1964 and 1982, more than two million injections of tartar emetic were administered each year to 250,000 Egyptians to combat schistosomiasis. On average patients received ten to twelve weekly IV injections with hastily sterilized syringes and needles. The result was a huge increase in hepatitis C, with half of the individuals aged forty and over testing positive for the virus in areas where the schistosomiasis treatment was administered. Similar iatrogenic transmission of hepatitis B occurred in the 1950s during the administration of IV drug treatments for syphilis and gonorrhea at STD clinics in Léopoldville. Of course, while such studies may lend support to Pepin’s theory, the evidence, such as it is, must be considered circumstantial and speculative. Like a jury presented with a murderer but no clear-cut murder weapon, we must weigh the evidence and decide who—or, in this case, what—is the most likely culprit.

  The first question a jury must address is why, given the fact that humans living in Cameroon, Gabon, Guinea, and Congo-Brazzaville have been in contact with chimpanzees infected with the SIV progenitor of HIV-1 for at least 2,000 years, an epidemic of HIV did not occur sooner? One answer is that in the precolonial period the lack of firearms made it more difficult to hunt apes and the dearth of roads through densely forested areas of Central Africa would have reduced interactions between humans and chimps. Even if, as seems likely, a bushmeat hunter was occasionally infected with HIV and managed to transmit the virus to his wife—or conversely, a cook infected her husband—the worst that might happen is that both would die of AIDS ten years later. Even if the couple were not monogamous, it is highly unlikely that in a remote village setting the virus would have spread far beyond the immediate community. Thus, in the precolonial period such infections would have represented epidemiological dead ends for the virus. However, around the turn of the nineteenth century, these epidemiological conditions began to change, creating new opportunities for progenitor HIV viruses to passage between people and be amplified more widely. The first development was the inauguration in 1892 of a steamship service from Léopoldville to Stanleyville (Kisangani) in the heart of the Congo. By connecting populations that had previously been largely separated, the service created the potential for viruses that might have died out in isolated, rural populations to reach growing urban centers. The population of Léopoldville received another boost in 1898 with the opening of the Matadi-Leo railway, prompting an influx of economic migrants and Belgian administrators. The result was that by 1923 Léopoldville had become the capital of the Belgian Congo. At around the same time, the city began hosting domestic flight
s and in 1936 inaugurated a direct international service to Brussels. More significant perhaps was the construction of new roads and railways by the French, including the 511-kilometer Chemin de Fer Congo-Ocean railroad. Connecting Brazzaville, on the opposite bank of the Congo River from Léopoldville, with Pointe-Noire on the coast, the railroad required the conscription of some 127,000 male laborers, resulting in the influx in the 1920s and 1930s of adult men into precisely the rural areas that were home to the chimpanzees that carried the progenitor of HIV-1. It also resulted in a constant passage of Africans and Europeans to and from Brazzaville, the new capital of the French federation.

  Once these rural-urban connections were up and running, it would not have taken very much to initiate a chain of sexual transmission in Brazzaville or Léopoldville. Pepin argues that one of the most important factors would have been the disruption of social relations that occurred during the colonial period. In particular, he points to the gender imbalances caused by the Belgian policy of conscripting large numbers of men into the labor force while discouraging their wives and families from leaving their villages. This was nowhere more pronounced than in Léopoldville, where by the 1920s men outnumbered women by 4 to 1—an imbalance that encouraged unmarried, working women known as “femme libres” to turn to part-time prostitution to supplement their income. Perhaps a bushmeat hunter traveled to Léopoldville and slept with one of these free women. Or perhaps a laborer on the railway alighted at Brazzaville and then caught a ferry to the opposite bank of the Congo River before making his way to a prostitute in Léopoldville. Or perhaps a migrant worker carried the virus to Brazzaville from higher up the Congo River, via one of its tributaries with Cameroon—the HIV-1 M group is most closely related to an SIV indigenous to chimpanzees from southeastern Cameroon; at the time of writing this is the favored scenario. The virus would have had an even greater chance of spreading if the person had earlier been treated for a tropical disease at one of the rudimentary hospitals near the railway and had contracted the virus from a contaminated syringe. This is not as far-fetched as it may sound. According to Pepin, the authorities were conducting campaigns against sleeping sickness and yaws along the railway in the 1930s, and in the same period southern Cameroon saw massive iatrogenic transmission of hepatitis C following the administration of intravenous quinine to treat malaria. Alternatively, the amplification effect could have occurred when an infected hunter presented himself at an STD clinic in Léopoldville to receive treatment for syphilis, or a prostitute infected by one of her clients presented herself for IV drug treatment at the same clinic. The prostitute would then have transmitted the virus sexually to her clients, and they in turn would have infected other sex workers, leading to an expanding circle of onward transmission and the gradual spread of HIV to other cities and towns in the Congo. The next amplifying effect would have come with independence from Belgium in 1960. As political chaos and civil war engulfed the Congo, thousands of refugees made their way to Kinshasa, resulting in a further expansion of prostitution. According to Pepin, it was this that most likely transformed HIV into a generalized epidemic; hence, the cases of AIDS that physicians encountered at the Mama Yemo hospital in the late 1970s and early 1980s. From Kinshasa, the virus was most likely spread by truckers and business travelers to other African cities and, afterwards, via planes to other countries and continents.

 

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