Anthropology Mini Essays

S hortly after the 1983 discovery of the human immunodeficiency vi - rus (HIV), the pathogen responsible for AIDS, investigators became aware of a strangely similar immune deficiency disease afflicting Asian monkeys (ma - caques) held in captivity in various U.S.

research labs. Soon, virologists identified the culprit: a simian immunodeficiency virus (SIV) that is found naturally in a West African monkey species, the sooty mangabey (Cercocebus atys), but is harm - less to that host. This virus, denoted SIVsm, is genetically similar to a weakly contagious form of the AIDS virus that is largely restricted to parts of West Africa, HIV-2, and thus is considered its likely precursor. More recent work has shown that the closest relative of the primary hu - man immunodeficiency virus (HIV-1) is another simian immunodeficiency virus, one carried by chimpanzees (SIVcpz). After comparing the SIVs in chimpan - zees and sooty mangabeys with HIV-1 and HIV-2 strains, investigators conclud - ed that there must have been multiple transmission “events” from simians to humans—at least seven for HIV-2 (some of which are known from only a single person who lives near mangabeys carry - ing a uniquely similar SIV) and three for HIV-1, the virus now infecting some 40 million people worldwide. How did SIVcpz and SIVsm cross over into humans and become patho - genic? Given the lack of historical refer - ences to AIDS-like disease in Africa pri - or to the mid-20th century, as well as its absence previously in the New World (which imported some 10 million Afri - can slaves during the 16th through 19th centuries), that transfer appears to have happened relatively recently—exactly when is a point of considerable debate.

And why did two distinct simian vi - ruses with which humans have appar - ently coexisted for centuries, or even millennia, suddenly pass into humans multiple times within a few decades? The answers to these questions have been slow in coming, despite the con - siderable efforts of molecular biologists to understand the nature and evolution of primate immunodeficiency viruses.

I am not one of those molecular biolo - gists; rather, I became a player in the field of AIDS-origin research through my interest in chimpanzee socioecol - ogy. Although I am partial to a theo - ry I helped to fashion for why AIDS emerged when it did, with time it might become clear that a competing idea bet - ter accounts for genesis of the epidemic.

Or perhaps the answer will prove to lie with some complex combination of fac - tors that no single explanation presently encompasses. Whatever the case, the solution almost certainly will come from one or more of four competing theories.

Theory 1: Tainted Polio Vaccine The first theory is the most controversial.

In a 1992 article in the magazine Rolling Stone , journalist Tom Curtis suggested that HIV could have resulted from the use in Africa of an experimental oral po - lio vaccine (OPV), one contaminated by a then-unknown SIV carried most prob - ably (Curtis supposed) by African green monkeys. Green-monkey kidney cells were widely used as a substrate to grow viruses for research and vaccine produc - tion. And one of the first major trials of an experimental oral polio virus vaccine took place from 1957 to 1960 in what are now the Democratic Republic of the Con - go, Burundi and Rwanda, seemingly the “hearth” of the global AIDS epidemic.

When interviewed by Curtis, Hilary Ko - prowski, the polio-vaccine pioneer who mounted that massive campaign, could not recall or find documentary evidence as to whether his group had used kid - ney cells from green monkeys or Asian macaques (which do not naturally carry an SIV). If culture media contained SIV (a possibility, given that the techniques available during that era were unable The Puzzling Origins of AIDS Although no one explanation has been universally accepted, four rival theories provide some important lessons Jim Moore Figure 1. Investigators puzzle over why the AIDS epidemic struck when it did. A simian virus very similar to HIV-1 (the HIV type re - sponsible for the vast majority of AIDS cases) is found in the chimpanzees of Central Africa, suggesting that these animals naturally harbor the progenitor virus. The leading idea is that this virus first passed through cuts to someone hunting or butchering a chimpanzee, but this theory alone cannot explain why the AIDS epidemic did not arise before the 20th century, because hunting chimpanzees for meat has presumably been going on for thousands of years. The author and two of his students sug - gested that the forced labor and population movements imposed on the natives of Central Africa during the colonial era—and the unster - ilized needles used in health campaigns as- sociated with those disruptions—might have created conditions favoring the transfer of the progenitor virus from chimpanzees to humans and its adaptation to become HIV. Vintage postcards show some relevant scenes from the region during the early part of the 20th century.

Clockwise from top: vaccination in the Congo Free State (now Democratic Republic of the Congo); Haute-Sangha (a province of what is now Central African Republic), doctor vacci - nates natives in the field; French Congo (now Republic of the Congo), missionaries vaccinate in the field in the vicinity of Brazzaville; Bel - gian Congo (now Democratic Republic of the Congo), construction of a bridge over a ravine. Jim Moore received his doctorate in biological an - thropology from Harvard in 1985, where he studied demography and sociality in primates. Since then he has been on the faculty of the University of Cali - fornia, San Diego, where his research focuses on primate behavioral ecology. Address: Anthropology Department, University of California, San Diego, La Jolla, CA 92093. Internet: [email protected] 2004 November–December 541 www.americanscientist.org © 2004 Sigma Xi, The Scientific Research Society. Reproduction with permission only. Contact [email protected].

© 2004 Sigma Xi, The Scientific Research Society. Reproduction with permission only. Contact [email protected]. 542 American Scientist, Volume 92 © 2004 Sigma Xi, The Scientific Research Society. Reproduction with permission only. Contact [email protected].

to guard against unknown viruses that did not cause overt symptoms in their monkey hosts), more than 900,000 peo - ple might have received it with their medicine, laying the basis for the current epidemic. Curtis credited this theory to Blaine Elswood, a Californian AIDS activist.

Interestingly, the idea that the admin - istration of a contaminated oral polio vaccine might have been involved in the genesis of AIDS was suggested independently by two others at about the same time. The first to do so was Louis Pascal, who like Elswood is not a scientist. After years of rejections, Pascal, a New Yorker, finally man - aged in 1991 to get the University of Wollongong in Australia to publish a paper describing his ideas. Not sur - prisingly, few noticed it. Attorney Walter Kyle also published a broadly similar theory in The Lancet , a British medical journal, in 1992. Since then, writer Edward Hooper, author of the controversial 1999 book The River, has become the contaminated-vaccine the - ory’s most ardent supporter. Hooper, noting a passing mention by Curtis of a chimpanzee colony run by Koprow- ski’s team, suggested that kidneys from these chimpanzees—not from green monkeys—may have been the original source of the virus. Multiple localized strains of HIV have now been discovered, and mass vac - cination appears unlikely to account for all of them. But the early distribution of the major pandemic strain, HIV-1 group M (for “main”), seems to fit reasonably well with the location of Koprowski’s campaigns, and the OPV theory now is applied primarily to this strain. Contamination of OPV is the only one of the four current theories that is read - ily falsifiable: Finding the HIV-1 group M virus in a tissue sample that predated the suspect vaccine would eliminate this possibility. So far that has not happened.

Still, many investigators give the theory little weight for other reasons, which has led to the widespread belief that the theory has been definitively disproved.

In 2001, for example, Science magazine published a piece titled “Disputed AIDS Theory Dies its Final Death,” and Na - ture ran one under the heading “Polio Vaccines Exonerated.” Earlier this year Nature also published “Origin of AIDS:

Contaminated Polio Vaccine Theory Re - futed”—a surprising title given that this theory ostensibly died three years ago. The recent findings of various mo - lecular biologists have indeed failed to provide support for the OPV theory. For example, in 2000 a few existing samples of the vaccine from Koprowski’s home institution (the Wistar Institute in Phila - delphia) were tested and found nega - tive for both chimpanzee DNA and SIV.

However, this result did not rule out the possibility, previously suggested by Hooper, that local amplification of the live-virus vaccine in Africa (to create more doses) could have introduced the SIV. The key issue is thus whether chim - panzee kidneys were used as a culture medium at any stage of Koprowski’s vaccine program. There is eyewitness testimony on both sides of this question, and failure to find SIVcpz in a handful of samples of the live vaccine strain of the type used in Africa does not prove the virus was absent in (putative) locally produced batches.

A second reason to question the OPV theory also came to light in 2000, with a report in Science by Bette T. Korber (of Los Alamos National Laboratory) and colleagues. They used molecular differ - ences among HIV-1 group M subtypes to estimate the date of their last com - mon ancestor. The conclusion: 1931 (with 95 percent confidence limits giv - ing the range 1915 to 1941), preceding OPV administration by decades. How - ever, the calculation of such common- ancestor dates can be thrown off by ge - netic recombination among subtypes (“viral sex”), which can make such dates come out too early, and there is increas - ing evidence that such recombination may be common with HIV. So maybe this date is not right. On the other hand, independent analyses using different methods have supported the date, and an analogous study of HIV-2 came up with an origin for the main group be - tween 1940 and 1945.

Another objection to the OPV the - ory concerns the subspecies of chim - panzee kept near Kisangani (formerly Stanleyville) at a facility called Camp Lindi, which Koprowski and colleagues maintain was used for safety-testing their vaccine, but which Hooper sus - pects was the source of chimpanzee tis - sues used to produce vaccine locally.

The SIVcpz strain that is most similar to HIV-1 has so far only been identified in a subspecies of chimpanzee native to west-central Africa, Pan troglodytes trog - lodytes . A second, less similar strain has been identified only in Pan troglodytes schweinfurthii , the subspecies found in east-central Africa—where Camp Lindi was located. The nearest known popu - lations of P. t. troglodytes are more than 500 kilometers from Koprowski’s chimp colony. So, this argument goes, the local - ly obtained captive chimps would not Figure 2. One controversial theory posits that the transfer of the chimpanzee immunodeficiency virus to human beings took place between 1957 and 1960 in the course of an oral polio-vaccination campaign carried out by Ghislain Courtois, Hilary Koprowski and their colleagues in what are now the Democratic Republic of the Congo, Burundi and Rwanda. This sign from the chimpanzee colony maintained in connection with that campaign reads, “Polio mission of Courtois-Koprowski, experi - mentation center, entrance forbidden.” (Photograph by Gilbert Rollais, courtesy of Edward Hooper.) 2004 November–December 543 www.americanscientist.org © 2004 Sigma Xi, The Scientific Research Society. Reproduction with permission only. Contact [email protected].

have been carrying the SIVcpz strain thought to have given rise to HIV-1.One difficulty with this argument is that distance is not always measured in kilometers, particularly in Central Afri - ca: Kisangani lies at the upstream end of the navigable portion of the Congo Riv - er, which borders the range of P. t. trog - lodytes for hundreds of kilometers, and river trade has been substantial since the colonial scramble for Africa in the late 19th century. If it became known that Americans were paying good money for young apes in Kisangani, it would be almost surprising if some hunters had not made the trip upriver. Anoth - er problem is the difficulty of proving the absence of something based on only a few samples, which requires some significant assumptions about the epidemiology of SIVcpz in the wild.

In short, although the majority of the biological evidence published in the last few years suggests that the OPV hypoth - esis is wrong, headlines reporting the death of this theory remain premature.

Theory 2: Cut Hunter The main competing theory posits that SIV is occasionally transmitted to hunters via blood-to-blood contact with an infected primate. Accord - ing to this view, the virus is usually cleared in its human host, but at least several times during the 20th century it survived and became established as HIV. It is not hard to imagine hunters suffering cuts or being injured by a wounded mangabey or chimpanzee, and some form of natural transfer be - tween species presumably accounts for the widespread distribution of SIVs in African primates. Hence, one has the “cut hunter” or “natural transfer” theory, which is probably the most ac - cepted idea today. According to that view, the timing of the widespread emergences of HIV-1 and HIV-2 in the middle part of the 20th century is at - tributed to urbanization and regional commerce, which create conditions ideal for spreading a sexually trans - mitted disease.

Unlike the case with OPV, there is no easy way to disprove this theory— even a smoking gun linking oral po - lio vaccines to HIV-1 group M would leave multiple other HIV strains unac - counted for, and “modernization” is a diffuse enough explanation to cover Dakar Kinshasa(Leopoldville) Nairobi Kisangani(Stanleyville) 5 (1976) 2 (1980/81) DEMOCRA TIC REPUBLIC OF THE CONG O Congo River RW A NDA BURUND I 8 (1980/81) 16 (1980/81) 3 (1980/81) KENYA SENEGAL ? 9 (1981) 1 (1981) African trials of CHAT vaccine 1957–1960 Burundi, unspecified CHA T vaccination sites number (and date) of confirmedHIV -1 infections in Africa through 1981 range ofPan troglodytes troglodytes range ofPan troglodytes schweinfurthii 1 (1959)2 (1970)1 (1975)1 (1978)16 (1980) 1 (1978) 1 (1977) 1 (1977) 1 (1976) Figure 3. “CHAT” oral polio vaccine was fed to approximately one million people at various sites (red dots and pink zone) between 1957 and 1960.

The degree of correspondence between these locales and early evidence of HIV-1 infection in Africa through 1981 (squares) is striking. The evidence comes either from patients who showed symptoms of AIDS and who later proved to be infected with HIV-1, or from HIV-positive blood samples taken at the time. (Note that two confirmed AIDS cases are not shown: a patient who acquired the virus somewhere in Tanzania before 1981, and one who acquired a form of the virus that is genetically distinct from the main form in either Cameroon or Kenya before 1967.) A comparison of CHAT sites and early AIDS cases that were never serologically tested (not shown) gives a similarly high degree of correspondence. Critics of the theory that this vaccination program ignited the epidemic note that the correlation between vaccination sites and early evidence of AIDS may just reflect the distribution of population centers and of medical facilities. They also point out that the SIVcpz carried by Pan troglodytes schweinfurthii (green) —the subspecies of chimpanzee found near Stanleyville (Kisangani), where those involved with the CHAT campaign maintained a colony of chimpanzees—is less closely related to HIV-1 than is the SIVcpz carried by Pan troglodytes troglodytes, which lives to the west (purple). The first criticism requires a careful statistical analysis to evaluate. The second ignores the fact that some chimpanzees might have been obtained for the colony from hunters working lower on the Congo River, which supported considerable steamer traffic at the time. (Data on CHAT sites and early HIV occurrences are from Hooper 2000. Subspecies ranges derived from Worobey et al. 2004.) 544 American Scientist, Volume 92 © 2004 Sigma Xi, The Scientific Research Society. Reproduction with permission only. Contact [email protected].

any of them. Nor is the cut-hunter theory particularly limited in time. Af - ter all, many Africans began moving to colonial capitals and ports in the 19th century. A hypothesis that does not account for the timing of the AIDS epidemic and that is not falsifiable is of limited use. Still, the thinness of the theory does not make it wrong Theory 3: Contaminated Needles The next proposal, a refinement of the cut-hunter theory, comes from Preston A. Marx, a virologist who holds posi - tions at Tulane University and at the Aaron Diamond AIDS Research Center. In 1995 he noted (to Hooper) that a big change in medical practice took place in the 1950s with the worldwide introduc - tion of disposable plastic syringes, mak - ing guaranteed sterile use possible and dropping the cost of syringe production by almost two orders of magnitude. The result was that the medical use of injec - tions went up astronomically. Because doses can be measured and there is no possibility of patients losing or selling the medicine, injections became a popu - lar way for doctors in the developing world to administer medicines, includ - ing vitamins, analgesics and other com - mon drugs.

The problem is that trivial costs are still large to someone living outside the cash economy, and plastic syringes cannot be sterilized by boiling: they melt. According to this scenario, the widespread availability of disposable syringes increased the acceptance of injections to treat a variety of diseases, but the syringes were not so available (or cheap) as to permit users actually to dispose of them. The result was that unsterilized syringes were used again and again, spreading viruses, including those that eventually be - came HIV.

Marx suggests that people’s immune systems would normally be able to over - come an SIV they acquired, say while butchering a monkey, within a week or two of infection. He further posits that the transition from SIV to HIV demands a series of mutations, with the probability of all the required mutations occurring being a function of viral population size.

Thus, Marx contends, some way must be found to permit the SIV to remain at high levels in people for long enough that such spontaneous mutations might take place.

He suggests that the required mechanism is “serial passaging” of virus through unsterile needles. That is, a cut hunter might get an injection while he is still har - boring large numbers of viral particles in his bloodstream; that same needle would then be used to infect another person, who might soon receive a second injec - tion, and so forth. High viral population levels can thus be maintained in a series of different people getting shots. With each transfer via contaminated needle, the virus finds itself in a fresh host, with an opportunity to proliferate before the infected person can mount an immune response. Chance mutations can thus ac - cumulate, and eventually the SIV adapts, becoming HIV. Theory 4:

Heart of Darkness Together with two undergraduate students, I am responsible for another variant to the cut-hunter theory, so perhaps I should explain how I be - came engaged in this field of inquiry.

In late 1998 I became involved in an Figure 5. Because the cut-hunter theory alone fails to explain the timing of the AIDS epi - demic, investigators have looked for other factors that might hold the key. One is the widespread distribution of disposable sy - ringes, which began in the 1950s. Although inexpensive, these devices proved too pre - cious to be thrown out in many poor parts of the world. And unlike the metal or glass units that they replaced, plastic syringes can - not be sterilized by boiling them (they melt).

The result is that unsterilized syringes were often reused, spreading disease. Even now, such problems are common in the develop - ing world, as can be seen in the proportion of health centers in selected African countries where syringes or needles are reused without sterilization. (Data from Dicko et al. 2000.) Figure 4. SIV may have crossed the species barrier to humans in the course of someone killing a chimpanzee or monkey for meat. At left, Efe Pygmy hunters of the Ituri Forest, Democratic Republic of the Congo, butcher a mangabey killed with bow and arrow. At right, a hunter from Sierra Leone uses a more modern weapon (a shotgun) to kill mangabeys. (Photograph at left by Heidi Verhoef, courtesy of the Bushmeat Crisis Task Force, www.bushmeat.org. Photograph at right courtesy of Glyn Davies, Zoological Society of London.) 0 20 40 60 80 1 00 Swaziland199 8 Uganda1998 Côte d’Ivoire 1997 Cha d 1997 proportion of health centers re-using syringes or needles without sterilization (percent) 2004 November–December 545 www.americanscientist.org © 2004 Sigma Xi, The Scientific Research Society. Reproduction with permission only. Contact [email protected].

e-mail discussion about the conser - vation implications of the identifica - tion of central African chimpanzees as the source of HIV-1, a result that Beatrice H. Hahn of the University of Alabama at Birmingham and her col - leagues had just published. At about the same time, a colleague urged me to read King Leopold’s Ghost , Adam Hoch - schild’s history of the Belgian Congo, and I was independently contacted by two students, Amit Chitnis and Diana Rawls, who were interested in doing something involving the intersection of biological anthropology and medi - cine. Then came the catalyst: an article in Discover magazine that mentioned the idea that the origin of AIDS might have had something to do with the chaos that followed colonial with - drawal from central Africa. The notion was that the colonial authorities had kept things under control, but when they left, “there was a free-for-all” that provided the conditions for the estab - lishment of a new disease.

King Leopold’s Ghost had more impact on me than any other book I have read. I had vaguely heard that Belgian rule was harsh, but I had not realized that more Africans probably died as a result of colonial practices in French Equatorial Africa and neighboring Belgian Congo between 1880 and the onset of World War II than had been taken from Africa as slaves during the preceding 400 years.

“Probably,” because no record was kept of the dead. The first censuses, taken in the 1920s, estimated that the popula - tion of the two colonies was then about 15 million. Census-takers recorded that wherever they asked, local people (co - lonial and native) reported that about twice as many had lived there two or three decades before, indicating that some 15 million had died. Losing 50 percent of the population exceeds even the 35-percent fatality rate of the Black Death in Europe. It seems Joseph Conrad’s Heart of Darkness was as much fact as fiction, and the horror described in that fa - mous novel reflected official policies in the Congo as much as individual insanity. What appeared to many as colonial “control” of the region in the late 19th and early 20th centu - ries brought chaos to the lives of the Africans who lived and died under it. Chitnis, Rawls and I set out to see what disease-promoting factors might have existed prior to the withdrawal of colonial powers around 1960. Candidates were not difficult to find, at least during the years prior to World War I. Forced labor camps of thousands had poor sanitation, poor diet and ex - hausting labor demands. It is hard to imagine better conditions for the estab - lishment of an immune-deficiency dis - ease. Where imagination fails, let history serve. To care for the health of the labor - ers, well-meaning but undersupplied doctors routinely inoculated workers against smallpox and dysentery, and they treated sleeping sickness with se - rial injections. The problem is, the mul - tiple injections given to arriving gangs of tens or hundreds were administered with only a handful of syringes. The im - portance of sterile technique was known but not regularly practiced: Transfer of pathogens would have been inevitable.

And to appease the laborers, in some of the camps sex workers were officially encouraged. And that was just the situation in the camps. Major efforts were made to erad - icate smallpox and sleeping sickness Figure 6. Another modification of the cut-hunter theory suggests that the widespread brutalization of natives of the Congo basin during the colonial era promoted both the adaptation of SIVcpz to humans (its transformation to HIV-1) and the initial spread of the virus. In particular, people living in this region suffered enormously, many being forced to extract ivory and rubber from the jungle.

King Leopold II of Belgium came under intense international scrutiny as a result of his harsh treatment of those living in the Congo Free State. This drawing, which appeared in the magazine Punch in 1906, shows a native man ensnared by a serpent with the head of King Leopold. Stock Montage 546 American Scientist, Volume 92 © 2004 Sigma Xi, The Scientific Research Society. Reproduction with permission only. Contact [email protected].

elsewhere in the region (these diseases cut into productivity). The shortage of syringes was acute. One 1916 sleep - ing-sickness control expedition treated 89,000 people in Ubangi Shari (now Central African Republic) using just six syringes. And before the introduction of dried smallpox vaccine in about 1914, the only way to transport vaccine to the interior was by serially inoculating people, traveling during the eight-day interval required for the new carrier to develop pustules from which the next inoculation could be derived. There are records of at least 14,000 people receiv - ing vaccine in this way. The method had been abandoned in Europe some 20 years before, because syphilis was all-too-often transmitted accidentally in the process.

Such circumstances easily could have promoted the evolution of HIV from SIVcpz. Imagine, for example, the fol - lowing scenario:

A fisherman flees his small village to es - cape a colonial patrol demanding its rub - ber quota; as he runs, he grabs one of the unfamiliar shotguns recently arrived in the area. While hiding for several days, he shoots a chimpanzee and, unfamiliar with the process of butchering it, is infected with SIVcpz. On return to the village he finds his family massacred and the village disbanded. He wanders for miles, dodging patrols, until arriving at a distant village.

The next day he is seized by a railroad press gang and marched for days to the labor site, where he (along with several hundred oth - ers) receives several injections for reasons he does not understand. During his months working on the railroad, he has little to eat and is continually stressed, susceptible to any infection. He finds some solace in one of the camp prostitutes (themselves imported by those in charge), but eventually dies of an undiagnosed wasting—the fate of hun - dreds in that camp alone. Disease, starva - tion, abuse—no record is kept, none of the authorities knows, and those few doctors who care are overwhelmed.

We wrote up a short article laying out reasons to at least examine colonial- era practices seriously in regard to how they may have contributed to the origin and spread of HIV. It probably would have been ignored but for another co - incidence: Our paper appeared in the journal AIDS Research and Human Retro - viruses almost simultaneously with the report of Korber and her colleagues in Science placing the beginnings of HIV-1 Group M in the early decades of the 20th century. If this dating is correct, the colo - nial-policy theory offers an explanation.

Note, however, that a version of the ba - sic cut-hunter theory that does not rely Figure 8. Until his death in 2000, William D.

Hamilton, a renowned evolutionary biolo - gist at the University of Oxford, was the most prominent scientist expressing support of the OPV theory. He died as an indirect result of malaria acquired in the Congo, where he and two coworkers were collecting material to probe the detailed nature of simian immunode - ficiency viruses in a region where chimpanzees were obtained in conjunction with the polio- vaccination campaigns of Koprowski and his colleagues. This photograph shows Hamilton in the field during his final expedition. Figure 7. Different theories point to different events as crucial to the genesis of the AIDS epidemic. The colonial-disruptions theory emphasizes goings-on in the early part of the 20th century, whereas the contaminated-needle theory places the spark after 1950. The controversial theory at - tributing the epidemic to an experimental polio-vaccination campaign carried out between 1957 and 1960 falls closest in time to the first confirmed HIV-positive blood sample, taken in 1959 from someone living in Leopoldville (Kinshasa). The number of people infected with HIV has since risen to almost 40 million. (Data on rise in HIV infections from UNAIDS.) Jeffrey B. Joy 1890 1900 1910 1920 1930 1940 1950 1960 1970 1980 19902000 1880 40 30 20 10 1879: King Leopold II of Belgium establishes first outpost in the Congo basin 1890: Joseph Conrad works on the Congo River, an experience that later inspired his novel Heart of Darkness 1908: Leopold’s Congo territory becomes a Belgian colony 1920s: a census reveals that 10 million have died in the Belgian Congo alone 1890 s –1913: Congolese natives suffered countless attrocities—murder, slavery and the severing of hands and feet—institutionalized crimes that Joseph Conrad, Mark Twain and Arthur Conan Doyle helped to expose 1950: introduction of disposable plastic syringes 1957: start of oral polio-vaccination campaign in Congo, Burundi, Rwanda 1959: first confirmed HIV infection (Leopoldville, Congo) 1982: the name “AIDS” is given to this newly emergent disease 1983: HIV discovered as cause of AIDS number of people living with HIV (millions) 2004 November–December 547 www.americanscientist.org © 2004 Sigma Xi, The Scientific Research Society. Reproduction with permission only. Contact [email protected].

on urbanization (or sets a much lower threshold for the critical level of city life) could also explain the genesis and initial spread of HIV during this period.Neither of these scenarios neatly ac - counts for the decades between the pos - tulated origin of HIV in the early part of the 20th century and the widespread emergence of AIDS in Africa, which did not take place until the early 1980s. But maybe that long delay is only an arti - fact of our perceptions: Starting with a single case and assuming a doubling in frequency every few years, one would need decades to pass for the prevalence to build appreciably; would colonial doctors have noticed an initially rare immune disease? Nor do these theo - ries readily explain details of the spa - tial pattern in the early cases of HIV infection and AIDS, which indeed show a suggestive overlap with the sites of oral polio vaccination. But is that cor - respondence just a function of the dis - tribution of population and doctors?

As with all of the current ideas, one can suggest various explanations to account for intriguing observations or troubling discrepancies. For the moment, the fit between theory and observation re - mains loose enough that no one view has proved absolutely compelling.

Battling Theories Arguments over rival theories of the origin of AIDS have raged viciously at times—far beyond the norms of most scientific debates. Indeed, both sides in the OPV controversy have in the re - cent scientific literature gone so far as to accuse their opponents of lying and manipulating evidence. I only became aware of the explosive nature of the debate after my students and I unwit - tingly wandered into this minefield.

Some of the participants in this con - troversy appear unwilling even to en - tertain the possibility of being wrong.

Given the precarious status of each of the current theories, it seems more rea - sonable to try to keep an open mind until better evidence emerges and, in the meantime, to consider the litera - ture on each of these origin stories as representing a highly refined simula - tion scenario. Insofar as there is any material benefit to come from under - standing the origin of HIV in terms of cautionary tales, each model can and should be considered plausible—and worrisome. After all, unsterile needles do transmit diseases, contaminated po - lio vaccine did spread a simian virus (one called SV40) to millions of people, doctors do sometimes conduct risky re - search, colonial policies did have major health consequences, and contact with wild animals can introduce pathogens into humans. An obvious general lesson can be drawn from all four theories: For some very puzzling reason, the origin of HIV was not fundamentally natural, given that humans apparently failed to ac - quire an immunodeficiency virus from simians during thousands of years of exposure. Instead, the emergence of HIV involved social change in one form or another: the abuses carried out at the hand of an invading foreign power; abrupt urbanization overwhelming the ability of medical and political authori - ties to manage the process; the undersu - pervised transfer of medical technology and half-measures in development pro - grams; doctors taking liberties in dis - tributing medicines without adequate precautions. It is worth noting that three of the four theories postulate an origin for AIDS that involves the inadvertent results of medical efforts, with what were then state-of-the-art health pro - grams and technologies carrying with them unforeseen dangers. Whether understanding the origin of HIV and AIDS is useful for evaluating risks associated with present-day con - cerns (say, the consumption of wildlife that might be the natural reservoir for emerging diseases like SARS, or evalu - ating the likelihood that the transplan - tation of animal organs into people will unleash a dangerous new virus) is a matter of opinion. My own view is that a firmer grasp of what happened in the past—and what might easily have hap - pened had circumstances been slightly different—helps society to understand these dangers and to minimize the risk of sparking the next global scourge.

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