The Chimp and the River: How AIDS Emerged from an African Forest

by David Quammen

  In mid-December, another e-mail from Hahn’s computer went out to Richard Wrangham, Jane Goodall, Martin Muller, and others. Under the subject line GOOD NEWS AT LAST, Hahn described the findings from Gimble and the position of his strain on the SIV family tree. Then, with her characteristic penchant for uppercase exuberance, she wrote: “THIS IS A HOME RUN!”

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  That was just the beginning. For nine years the study continued. Fieldworkers at Gombe collected fecal samples from ninety-four different chimpanzees, each of which was known by name and, in most cases, by its individual character and family history. Beatrice Hahn’s people did the analyses, finding that seventeen of those ninety-four chimps were SIV-positive. As time passed, some chimps died. Others disappeared in the forest and were presumed dead when they failed to reappear. Death is often a private matter for wild creatures, including chimpanzees, especially when it comes upon them by slow and painful degrees. They tend to go absent from the social group, if there is a social group, and meet the end alone. Gimble last showed himself to trackers on January 23, 2007. His body was never found.

  Back in Birmingham, there was turnover of a different sort, as grad students and postdocs cycled through Hahn’s lab. Mario Santiago departed, heading off for the next stage of his career, and Brandon Keele arrived. Samples continued coming from Gombe, in occasional batches, and those samples were analyzed—a slow and laborious process. Much of the work fell to Keele, though even for him this was “a backburner project.” Keele described to me, during my visit with him at Fort Detrick, the moment of recognition that occurred near the end of his postdoc period, bringing that project to the front burner.

  “I was trying to leave and finish up. I said to myself, ‘I wonder what’s happening with these chimps?’” He was aware that the number of known SIV-positives at Gombe had increased as the sampling stretched on, and that there was evidence of vertical transmission (mother to infant) as well as sexual transmission accounting for new infections. He thought the study might yield an interesting, undramatic paper about how a harmless virus spreads through a population. “And then we started compiling the data,” he told me. That meant bringing in a dimension of behavioral observations from the field. So he contacted collaborators at the Jane Goodall Institute’s research headquarters in Minnesota and, asking about one individual after another, heard a drumbeat of unsettling news.

  “Oh, no, that chimp is dead.”

  “No, that chimp is dead. He died in 2006.”

  “No, that chimp is dead.”

  Keele recalled asking himself: “What the hell is going on?” Part of the answer, revealed when he saw an updated mortality list, was that a wave of untimely deaths had been sweeping through SIV-positive members of the Gombe population.

  He and the team at Hahn’s lab had recently written an abstract for a talk he planned to give at a meeting, which would lead in time to a journal publication. The draft abstract, by Keele’s recollection, contained a sentence such as: “It doesn’t really seem that there is a death hazard to infection in these chimps.” They had sent the draft to their partners at Gombe, who responded quickly with news of seven additional chimpanzee deaths, about which Keele hadn’t even known. He scrapped the abstract, thought again about what he was doing, and began working more closely with Gombe and Minnesota to assemble a more complete set of data. Then they would see where it led.

  Around the same time, spring of 2008, Keele also heard about some unusual pathology results on tissues from one dead Gombe chimp. The chimp was known as Yolanda, a twenty-four-year-old female. She sickened in November 2007, of an unknown ailment, and came down from the mountains to languish near the research center. People tried to feed her, but Yolanda didn’t eat. She sat in the rain amid thick vegetation, weakened and miserable, and then died. They put her body in a freezer. Two months later, it was thawed for necropsy.

  The necropsy was performed by Jane Raphael, a Tanzanian veterinarian working at the Gombe Stream Research Center and specially trained for the task. Not knowing whether Yolanda had been SIV-positive, Raphael took the stipulated precautions. She wore a full Tyvek suit, two layers of gloves, an N95 respirator mask, a face shield, and rubber boots. She split open Yolanda’s belly, cut through the ribs, and spread them wide to see what she could see.

  “The main problem was in the abdominal cavity,” Raphael told me, two years later, as we sat in her small office just up from the shore of Lake Tanganyika. “There was something like abdominal peritonitis. The intestines were very much adhered together.” Raphael, a quiet woman, wearing a neat cornrow hairdo and a flowered print dress, chose her words carefully. She described separating the glommed guts with her gloved hands. “It was unusual,” she said. She seemed to remember it all vividly. “The muscles underneath the pelvis were very much inflamed. Red. And they had some blackish spots.” What caused the inflammation? Judiciously empirical, Raphael said she didn’t know.

  Her inspection done, she had snipped out tissue samples from virtually every organ: spleen, liver, intestines, heart, lungs, kidneys, brain, lymph nodes. For the SIV-positive cases, she said, lymph nodes were especially important. Yolanda’s lymph nodes appeared normal to the eye, but histopathology would later penetrate that illusion. Some of the samples, preserved in RNAlater, went off to Beatrice Hahn. Others, pickled in formalin, were destined for a pathologist in Chicago. When the results came together, this case would challenge prevailing ideas about SIV in chimpanzees. “Previously it was said, they are infected but they don’t come down with the disease,” Raphael told me. “Yolanda made us to start thinking otherwise.”

  I followed the pickled samples to Chicago, where the pathologist who had examined them, Karen Terio, welcomed me to a glimpse of the evidence. Terio trained as a veterinarian, at one of the country’s best vet schools, then did a residency and a doctorate in pathology, specializing in diseases transferred between species. She worked for the University of Illinois and consulted for the Lincoln Park Zoo, which helps run a health-monitoring project at Gombe. Hence the lymph nodes and other bits of Yolanda came for her expert scrutiny. Terio cut up the tissues, sent them to laboratory technicians for mounting and staining, then sat down for a look at the slides. “It was striking because I couldn’t find any lymphocytes,” she told me. “When I saw the first lymph node, I thought, ‘Hmm, this is weird.’” She asked her boss to have a look through the microscope. He did, and agreed there was something very wrong. She phoned a colleague at the Lincoln Park Zoo, Elizabeth Lonsdorf, who leads the zoo’s work on behalf of wild African apes, including the health project at Gombe.

  “We have a problem,” Terio told Lonsdorf. “She doesn’t have any lymphocytes.”

  “Does that mean what I think it means?”

  “Yes. The lesions in this animal look like an end-stage AIDS patient.”

  Together she and Lonsdorf made a call to Beatrice Hahn. Hahn’s first question was, “Are you sure?” Terio was indeed sure, but she quickly e-mailed images of the slides so that the others could judge for themselves. Brandon Keele was by now in the loop. Terio sent actual slides to another collaborator, an expert on immune-system pathology, to refine the diagnosis. Everyone agreed and, with the sample code broken, everyone knew how these pieces fit together: The chimp Yolanda, dead at age twenty-four, had been SIV-positive and suffering immunodeficiency.

  Inviting me to a chair at her big double-viewer Olympus microscope, Karen Terio brought out the same slides she had shared with Hahn and Lonsdorf. From her place at the scope she could manipulate a cursor, a little red arrow, moving it over the field to point out what we were seeing. First she showed me a thin-slice section from a lymph node of a normal, SIV-negative chimpanzee. This was for comparison. It looked like a peat bog as viewed on Google Earth, bulging and rife with sphagnum and huckleberry, thick, rich, and riddled just slightly with narrow spaces resembling small sloughs and creeks. The tissue was stained magenta and heavily speckled with darker blue dots. The dots, Terio explained, wer
e lymphocytes in their healthy abundance. In an area where they’re especially dense, they pack together into a follicle, like a bag full of jellybeans. She jabbed her red arrow at a follicle.

  Then she placed another slide into viewing position. The slide held a slice from one of Yolanda’s lymph nodes. Instead of a peat bog, it looked like scrub desert slashed by a large drywash, many days since the last rain.

  “Mmmm,” I said.

  “This is essentially the connective tissue,” Terio said. She meant that it was supportive structure only, minus the working innards. Sere and empty. “We’ve got very, very few lymphocytes left in this animal.”

  “Yeah.”

  “And it’s collapsed. You see, this whole thing has just sort of collapsed on itself, ’cause there’s nothing in there to hold it up.” Her little red arrow wandered forlorn through the desert. No sphagnum, no follicles, no little blue dots. I imagined Karen Terio, back in April 2008, examining these slides on her lonesome—and encountering such evidence, before anyone else, at a time when the illusion of nonpathogenic SIVcpz was embraced by researchers everywhere.

  “So you sat there, and looked at this . . .”

  “And went, ‘Oh, no,’” she said.

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  Terio’s findings, plus the field data from Gombe, plus the molecular analyses from Hahn’s lab—these all came together in a paper published by Nature during the summer of 2009. Brandon Keele was first author; Beatrice Hahn was last. “Increased Mortality and AIDS-like Immunopathology in Wild Chimpanzees Infected with SIVcpz” was the catchy title. I think of it—and I’m not alone—as “the Gombe paper.” The long list of coauthors included Karen Terio, Terio’s boss, Elizabeth Lonsdorf, Jane Raphael, two of Hahn’s senior colleagues, the expert on primate cell pathology, the chief scientist at Gombe, and Jane Goodall herself.

  “Well, I sort of had to be. But I had these long talks with Beatrice first,” Jane told me. “She was going to publish it anyway.” In the sweep of inevitability and the name of science, Dr. Goodall signed on.

  The paper’s salient conclusion was that, contrary to Keele’s earlier draft abstract, there is indeed a death hazard for SIV-positive chimps at Gombe. Of the eighteen individuals that died during the study period, seven were SIV-positive. Given that less than 20 percent of the population was SIV-positive, and adjusted for normal mortality at a given age, this reflected a risk of death ten times to sixteen times higher for SIV-positive chimps than for SIV-negatives. Repeat: ten to sixteen times higher. The total numbers were small but the margin was significant. Infected animals were falling away. Furthermore, SIV-positive females had lower birth rates and greater infant mortality. Further still, three necropsied individuals (including Yolanda, though her name wasn’t mentioned) showed signs of lymphocyte loss and other damage resembling end-stage AIDS.

  The authors suggested, cautiously but firmly, “that SIVcpz has a substantial negative impact on the health, reproduction and lifespan of chimpanzees in the wild.” So it’s not a harmless passenger. It’s a hominoid killer. Their problem as well as ours.

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  Here’s what you have come to understand. That the AIDS pandemic is traceable to a single contingent event. That this event involved a bloody interaction between one chimpanzee and one human. That it occurred in southeastern Cameroon, around the year 1908, give or take. That it led to the proliferation of one strain of virus, now known as HIV-1 group M. That this virus was probably lethal in chimpanzees before the spillover occurred, and that it was certainly lethal in humans afterward. That from southeastern Cameroon it must have traveled downriver, along the Sangha and then the Congo, to Brazzaville and Léopoldville. That from those entrepôts it spread to the world.

  Spread how? Once it reached Léopoldville, the group M virus seems to have entered a vortex of circumstances unlike anything at the headwaters of the Sangha. It differed from HIV-2 biologically (having adapted to chimpanzee hosts) and it differed from groups N and O by chance and opportunity (having found itself in an urban environment). Whatever happened to it in Léopoldville during the first half of the twentieth century can only be conjectured. Population density of potential human hosts, a high ratio of males to females, sexual mores different from what prevailed in the villages, and prostitution—these were all parts of the mix. But sex plus crowding may not be a sufficient explanation. A fuller chain of conjecture, and maybe a better one, has been offered by Jacques Pepin, a Canadian professor of microbiology who, during the 1980s, worked for four years at a bush hospital in Zaire. Pepin coauthored several journal papers on the subject and, in 2011, published a book titled The Origins of AIDS. Having added some deep historical research to his own field experience and microbiological expertise, he proposed that the crucial factor intermediating between the Cut Hunter and the global pandemic was the hypodermic syringe.

  Pepin wasn’t referring to recreational drugs and the works shared by addicts at shooting galleries. In a paper titled “Noble Goals, Unforeseen Consequences,” and then at greater length in his book, he pointed instead to a series of well-intended campaigns by colonial health authorities, between 1921 and 1959, aimed at treating certain tropical diseases with injectable medicines. There was a massive effort, for instance, against trypanosomiasis (sleeping sickness) in Cameroon. Trypanosomiasis is caused by a persistent little bug, Trypanosoma brucei, transmitted in the bite of tsetse flies. The treatment in those years entailed injections of arsenical drugs such as tryparsamide—and a patient didn’t get just one shot but a series. In Gabon and Moyen-Congo (the French colonial name for what’s now the Republic of the Congo), the regimen for trypanosomiasis sometimes entailed thirty-six injections over three years. And there were similar efforts to control syphilis and yaws. Malaria was treated with injectable forms of quinine. Leprosy patients, in that era before oral antibiotics, underwent a course of injections with extract of chaulmoogra (an Indian medicinal plant), two or three shots per week for a year. In the Belgian Congo, mobile teams of injecteurs, people with no formal education but a small bit of technical training, visited trypanosomiasis patients in their villages to give weekly shots. It was a period of mania for the latest medical wonder: needle-delivered cures. Everyone was getting jabbed.

  Of course, this was long before the era of the disposable syringe. Hypodermic syringes, for injecting medicines into muscles or veins, were invented in 1848 and, until after World War I, were handmade of glass and metal by skilled craftsmen. They were expensive, delicate, and meant to be reused like any other precision medical instrument. During the 1920s their manufacture became mechanized, to the point where 2 million syringes were produced globally in 1930, making them more available but not more expendable. To the medical officers working in Central Africa at that time, they seemed invaluable but were in short supply. A famous French colonial doctor named Eugène Jamot, working just east of the upper Sangha River (in a portion of French Equatorial Africa then known as Oubangui-Chari) during 1917–1919, treated 5,347 trypanosomiasis cases using only six syringes. This sort of production-line delivery of injectable medicines didn’t allow time for boiling a syringe and needle between uses. It’s difficult now, based on skimpy sources and laconic testimony, to know exactly what sort of sanitary precautions were taken. But according to one Belgian doctor, writing in 1953: “The Congo contains various health institutions (maternity centres, hospitals, dispensaries, etc.) where every day local nurses give dozens, even hundreds, of injections in conditions such that sterilisation of the needle or the syringe is impossible.” This man was writing about the risk of accidental transmission of hepatitis B during treatment for venereal diseases, but Pepin quoted his report at length, for its potential relevance to HIV:

  The large number of patients and the small quantity of syringes available to the nursing staff preclude sterilisation by autoclave after each use. Used syringes are simply rinsed, first with water, then with alcohol and ether, and are ready for a new patient. The same type of procedure exists in all health instituti
ons where a small number of nurses have to provide care to a large number of patients, with very scarce supplies. The syringe is used from one patient to the next, occasionally retaining small quantities of infectious blood, which are large enough to transmit the disease.

  How much of this went on? Very much. Pepin’s diligent search through old colonial archives turned up some big numbers. In the period 1927–1928, Eugène Jamot’s team in Cameroon performed 207,089 injections of tryparsamide, plus about a million injections of something called atoxyl, another arsenical drug for treating trypanosomiasis. During just the year 1937, throughout French Equatorial Africa, the army of doctors and nurses and semipro injectors delivered 588,086 needlesticks aimed at trypanosomiasis, not to mention countless more for other diseases. Pepin’s arithmetic totaled up 3.9 million injections just against trypanosomiasis, of which 74 percent were intravenous (right into a vein, not just a muscle), the most direct method of drug delivery and also the best for unintentionally transmitting a blood-borne virus.

  All those injections, according to Pepin, might account for boosting the incidence of HIV infection beyond a critical threshold. Once the reusable needles and syringes had put the virus into enough people—say, several hundred—it wouldn’t come to a dead end, it wouldn’t burn out, and sexual transmission could do the rest. Some experts, including Michael Worobey and Beatrice Hahn, doubt that needles were necessary in any such way to the establishment of HIV in humans—that is, to its early transmission from one person to another. But even they agree that injection campaigns could have played a role later, spreading the virus in Africa once it was established.

  This needle theory didn’t originate with Jacques Pepin. It dates back more than a decade to work by an earlier team of researchers, including Preston Marx of the Rockefeller University, who proposed it in 2000 at the same Royal Society meeting on AIDS origins at which Edward Hooper spoke for his oral polio vaccine theory. Marx’s group even argued that serial passage of HIV through people, by means of such injection campaigns, might have accelerated the evolution of the virus and its adaptation to humans as a host, just as experimentally passaging some other virus through a series of laboratory mice might assist its adaptation to, and increase its transmissibility among, mice. Jacques Pepin picked up where Preston Marx left off, though with less emphasis on the evolutionary effect of serial passage. Pepin’s main point was simply that dirty needles, used so widely, must have raised the prevalence of the virus among people in Central Africa. Unlike the OPV theory, this one hasn’t been discredited by further research, and Pepin’s new archival evidence suggests that it’s highly plausible, if unprovable.