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

  THE

  CHIMP

  AND THE

  RIVER

  How AIDS Emerged

  from an African Forest

  DAVID QUAMMEN

  W. W. Norton & Company

  New York • London

  To the men and women who have suffered this disease and those who continue to suffer it

  CONTENTS

  Introduction

  The Chimp and the River

  Notes

  Bibliography

  Acknowledgments

  Index

  INTRODUCTION

  AIDS has been written about many times, from many angles, but the story as told here is drastically different from any version you are likely to have read, heard about, or otherwise absorbed. The main difference is that this is an account of the ultimate source of the pandemic. It’s essentially an ecological narrative rather than a medical one—by which I mean that it turns on the interaction of three kinds of creature: chimpanzee, human, and virus. I have tried to describe how, when, and where the virus in question (HIV-1 group M, the pandemic strain), which was previously unknown among people, got its start in the human population. There was a single point in space and time. There was a fateful event. The world became cognizant of AIDS in the early 1980s, of course, but that wasn’t the beginning—far from it. The real moment of origin occurred decades earlier and thousands of miles away. It’s now possible to say, based on persuasive research in molecular genetics, as published in scientific journals but little noticed by the public, that the virus passed from a single chimpanzee into a single person, during a presumably bloody encounter, in the southeastern corner of Cameroon, near a minor tributary of the Congo River, around 1908, give or take a margin of error. Key components of that research were led by Beatrice Hahn, then of the University of Alabama at Birmingham, and Michael Worobey, at the University of Arizona, both of whom feature in this little book.

  In The Chimp and the River I trace backward to that moment of origin, reconstruct it, and then follow its consequences forward again, along the pathways of social history, epidemiology, and dolorous accident, to the point when AIDS “suddenly” emerged as a global human disaster.

  AIDS is horrible and unique, but it’s also part of a larger pattern. Everything comes from somewhere, and strange new infectious diseases, emerging abruptly among humans, come mostly from nonhuman animals. The disease might be caused by a virus, or a bacterium, or a protozoan, or some other form of dangerous bug. That bug might live inconspicuously in a kind of rodent, or a bat, or a bird, or a monkey, or an ape. Crossing by happenstance from its animal hideaway into its first human victim, it might find surprisingly hospitable conditions; it might replicate aggressively and abundantly; it might cause illness, even death; and in the meantime, it might pass onward from its first human victim into others. There’s a fancy term for this phenomenon, used by scientists who study infectious diseases from an ecological perspective: zoonosis. A zoonosis is an animal infection transmissible to humans. The animal hideaway is known as a reservoir host. The event of transmission, from one species into another, is called spillover.

  That bit of terminology gave me the title for my 2012 book, Spillover: Animal Infections and the Next Human Pandemic, in which The Chimp and the River first appeared as a long chapter. I revised that material here just enough to make it a self-contained narrative with its own wider meaning and its own dire implication. Its wider meaning is that pandemic AIDS resulted from our dealings with the natural world, as well as from our dealings with one another. Its dire implication is that, having happened once catastrophically, and at least eleven other times (as you’ll learn from this story) less consequentially, the spillover of an HIV-like virus from nonhuman primates to humans is not a highly improbable event. It could certainly happen again.

  Spillover is a book about zoonotic diseases and their increasing importance in our modern world—a world where 7 billion humans interact ever more frequently, ever more disruptively, with the wild animals that live in wild places. Roughly 60 percent of the infectious diseases known among humans are zoonotic in the strict sense, coming to us continually or within recent history from animals; most if not all of the other 40 percent, including human afflictions such as measles and smallpox, can be considered zoonotic in a broader sense, given that we are a relatively young species and our tormenting bugs have their own histories that precede us. Everything, as I’ve said, and will say again, comes from somewhere.

  My lengthy treatment of this subject, in Spillover, focuses on a selection of nasty diseases, some new and some old, some infamous and some obscure, and on the viruses and other microbes that cause them: Ebola in Africa, Nipah in Bangladesh and Malaysia, SARS as it came out of China, Lyme disease in the suburbs of New England, Hendra amid the horse cultures of Australia, zoonotic malaria in Borneo, influenza everywhere, and a few others. SARS killed about eight hundred people during its frightening emergence back in 2003, but then it was controlled by good science and rigorous public health measures, and the SARS virus has not re-emerged since. Ebola virus disease is gruesome and highly lethal but its geographical reach and its total of human victims, so far, have been relatively small (although, at the time of this writing, the reach of Ebola has increased alarmingly during the 2014 outbreak in West Africa; no one yet knows where that will end). Lyme disease is punishingly familiar to many people but it doesn’t usually kill them. Nipah has re-emerged repeatedly in Bangladesh, usually when the seasonal harvest of date-palm sap has brought sap harvesters and their customers into unhealthy contact with the excretions of bats. Hendra can be terrifying if you’re an Australian who works with horses, but it has killed fewer than ten people since its first known occurrence in 1994. Given the limited scope and peculiarities of such problems, why should people around the rest of the world concern themselves with the subject of zoonotic disease?

  It’s a fair question but there are good answers. Some of those answers are intricate and speculative. Others are objective and blunt. The bluntest is this: AIDS.

  THE

  CHIMP

  AND THE

  RIVER

  1

  There are multiple beginnings to what we think we know about the AIDS pandemic, most of which don’t even address the subject of its ultimate origin in a single chimpanzee.

  For instance: In autumn of 1980, a young immunologist named Michael Gottlieb, an assistant professor at the UCLA Medical Center, began noticing a strange pattern of infections among certain male patients. The patients, eventually five of them, were all active homosexuals and all suffering from pneumonia caused by a usually harmless fungus then known as Pneumocystis carinii. (Nowadays, after a name change, it’s Pneumocystis jurovecii.) The stuff is ubiquitous; it floats around everywhere. Their immune systems should have been able to clear it. But their immune systems evidently weren’t working, and this fungus filled their lungs. Each man also had another sort of fungal infection—oral candidiasis, meaning a mouthful of slimy Candida yeast, more often seen in newborn babies, diabetics, and people with compromised immune systems than in healthy adults. Blood tests, done on several of the patients, showed dramatic depletions of certain lymphocytes (white blood cells) that are crucial in regulating immune responses. Specifically, it was thymus-dependent lymphocytes (T cells, for short) that were “profoundly depressed” in number. Although Gottlieb noted some other symptoms, those three stood out: Pneumocystis pneumonia, oral candidiasis, dearth of T cells. In mid-May of 1981, he and a colleague wrote a brief paper, with cooperation from other Los Angeles doctors, describing th
eir observations. They didn’t speculate about causes. They just saw the pattern as a befuddling, ominous trend and felt they should publish quickly. An editor at The New England Journal of Medicine was interested but his lead time would be at least three months.

  So Gottlieb turned to the streamlined newsletter of the Centers for Disease Control (as that agency was then known) in Atlanta. The CDC issues Morbidity and Mortality Weekly Report to deliver breaking news of disease events in a timely way. Gottlieb’s barebones text, less than two pages long, appeared in MMWR on June 5, 1981, under the dry title “Pneumocystis Pneumonia—Los Angeles.” It was the first published medical alert about a syndrome that didn’t yet have a name.

  The second alert came a month later, again in the CDC newsletter. While Gottlieb noticed Pneumocystis pneumonia and candidiasis, a New York dermatologist named Alvin E. Friedman-Kien spotted a parallel trend involving a different disease: Kaposi’s sarcoma. A rare form of cancer, not usually too aggressive, Kaposi’s sarcoma was known primarily as an affliction of middle-aged Mediterranean males—the sort of fellows you’d expect to find in an Athens café, drinking coffee and playing dominoes. This cancer often showed itself as purplish nodules in the skin. Within less than three years, Friedman-Kien and his network of colleagues saw twenty-six cases of Kaposi’s sarcoma in youngish homosexual men. Some of those patients also had Pneumocystis pneumonia. Eight of them died. Hmm. Morbidity and Mortality Weekly Report carried Friedman-Kien’s communication on July 3, 1981.

  Kaposi’s sarcoma also figured prominently in a set of clinical observations made in Miami around the same time. The symptoms among this group of patients were similar; the cultural profile was different. These sick people, twenty of them, hospitalized between early 1980 and June 1982, were all Haitian immigrants. Most had arrived in the United States recently. By their own testimony during medical interviews they were all heterosexuals, with no history of homosexual activity. But their cluster of ailments resembled what Gottlieb had seen among gay men in Los Angeles and Friedman-Kien among gay men in New York: Pneumocystis pneumonia, candidiasis in the throat, plus other unusual infections, irregularities in lymphocyte counts, and aggressive Kaposi’s sarcoma. Ten of the Haitians died. The team of doctors who published these observations saw a “syndrome” that seemed “strikingly similar to the syndrome of immunodeficiency described recently among American homosexuals.” The early connection to Haitian heterosexuals would later come to seem like a false lead and be largely ignored in discussions of AIDS. It was hard to confirm, given the limits of interview data, and harder still to construe. Calling attention to it even came to seem politically incorrect. Then, later still, its real significance would emerge from work at the level of molecular genetics.

  Another perceived starting point was Gaëtan Dugas, the young Canadian flight attendant who became notorious as “Patient Zero.” You’ve heard of him, probably, if you’ve heard much of anything about the dawning of AIDS. Dugas has been written about as the man who “carried the virus out of Africa and introduced it into the Western gay community.” He wasn’t. But he seems to have played an oversized and culpably heedless role as a transmitter during the 1970s and early 1980s. As a flight steward, with almost cost-free privileges of personal travel, he flew often between major cities in North America, joining in sybaritic play where he landed, notching up conquests, living the high life of a sexually voracious gay man at the height of the bathhouse era. He was handsome, sandy-haired, vain but charming, even “gorgeous” in some eyes. According to Randy Shilts, author of And the Band Played On (which includes much heroic research and a bit of questionably reliable reimagining), Dugas himself reckoned that in the decade since becoming actively gay he had had at least twenty-five hundred sexual partners. Dugas paid a price for his appetite and his daring. He developed Kaposi’s sarcoma, underwent chemotherapy for that, suffered from Pneumocystis pneumonia and other AIDS-related infections, and died of kidney failure at age thirty-one. During the brief stretch of years between his Kaposi’s diagnosis and his final invalidism, Gaëtan Dugas didn’t slow down. But he seems to have tipped, in his lonely despair, from hedonism to malice; he would have sex with a new acquaintance at the Eighth-and-Howard bathhouse in San Francisco, then turn up the lights—so Randy Shilts claimed—display his lesions, and say: “I’ve got gay cancer. I’m going to die and so are you.”

  In the same month as Dugas’s death, March 1984, a team of epidemiologists from the CDC published a landmark study of the role of sexual contact in linking cases of what by then was called AIDS. The world had a label now but not an explanation. “Although the cause of AIDS is unknown,” wrote the CDC team, whose lead author was David M. Auerbach, “it may be caused by an infectious agent that is transmissible from person to person in a manner analogous to hepatitis B infection.” Hepatitis B is a blood-borne virus. It moves primarily by sexual contact, intravenous drug use with shared needles, or transfusion of blood products carrying the virus as a contaminant. It seemed like a template for understanding what otherwise was still a bewildering convergence of symptoms. “The existence of a cluster of AIDS cases linked by homosexual contact is consistent with an infectious-agent hypothesis,” the CDC group added. Not a toxic chemical, not an accident of genetics, but some kind of bug, is what they meant.

  Auerbach and his colleagues had gathered information from nineteen AIDS cases in southern California, interviewing each patient or, if he was dead, his close companions. They spoke with another twenty-one patients in New York and other American cities, and from their forty case histories they created a graphic figure of forty interconnected disks, like a Tinkertoy structure, showing who was linked sexually with whom. The patients’ identities were coded by location and number, such as “SF 1,” “LA 6,” and “NY 19.” At the center of the network, connected directly to eight disks and indirectly to all the rest, was a disk labeled “0.” Although the researchers didn’t name him, that patient was Gaëtan Dugas. Randy Shilts later transformed the somewhat bland “Patient 0,” as mentioned in this paper, to the more resonant “Patient Zero” of his book. But what the word “Zero” belies, what the number “0” ignores, and what the central position of that one disk within the figure fails to acknowledge, is that Gaëtan Dugas didn’t conceive the AIDS virus himself. Everything comes from somewhere, and he got it from someone else. Dugas himself was infected by some other human, presumably during a sexual encounter—and not in Africa, not in Haiti, somewhere closer to home. That was possible because, as evidence now shows, HIV had already arrived in North America when Gaëtan Dugas was a virginal adolescent.

  It had also arrived in Europe, though on that continent it hadn’t yet gone far. A Danish doctor named Grethe Rask, who had been working in Africa, departed in 1977 from what was then Zaire and returned to Copenhagen for treatment of a condition that had been dragging her downward for several years. During her time in Zaire, Rask first ran a small hospital in a remote town in the north, then served as chief surgeon at a large Red Cross facility in the capital, Kinshasa. Somewhere along the way, possibly during a surgical procedure done without adequate protective supplies (such as rubber gloves), she became infected with something for which no one at the time had a description or a name. She felt ill and fatigued. Drained by persistent diarrhea, she lost weight. Her lymph nodes swelled and stayed swollen. She told a friend: “I’d better go home to die.” Back in Denmark, tests revealed a shortage of T cells. Her breath came with such difficulty that she depended on bottled oxygen. She struggled against staph infections. Candida fungus glazed her mouth. By the time Grethe Rask died, on December 12, 1977, her lungs were clogged with Pneumocystis carinii, and that seems to have been what killed her.

  It shouldn’t have, according to standard medical wisdom. Pneumocystis pneumonia wasn’t normally a fatal condition. There had to be a broader explanation, and there was. Nine years later, a sample of Rask’s blood serum tested positive for HIV.

  All these unfortunate people—Grethe Rask, Gaëta
n Dugas, the five men in Gottlieb’s report from Los Angeles, the Kaposi’s sarcoma patients known to Friedman-Kien, the Haitians in Miami, the cluster of thirty-nine (besides Dugas) identified in David Auerbach’s study—were among the earliest recognized cases of what has retrospectively been identified as AIDS. But they weren’t among the first victims. Not even close. Instead they represent midpoints in the course of the pandemic, marking the stage at which a slowly building, almost unnoticeable phenomenon suddenly rose to a crescendo. The real beginning of AIDS lay elsewhere, and more decades passed while a few scientists worked to discover it.

  2

  In the early years after its detection, the new illness was a shifting shape that carried several different names and acronyms. GRID was one, standing for Gay-Related Immune Deficiency. That proved too restricted as heterosexual patients began to turn up: needle-sharing addicts, hemophiliacs, other unlucky straights. Some doctors preferred ACIDS, for Acquired Community Immune Deficiency Syndrome. The word “community” was meant to signal that people acquired it out there, not in hospitals. A more precise if clumsier formulation, favored briefly by the CDC’s Morbidity and Mortality Weekly Report, was “Kaposi’s sarcoma and opportunistic infections in previously healthy persons,” which didn’t abbreviate neatly. KSOIPHP lacked punch. By September 1982, MMWR had switched its terminology to Acquired Immune Deficiency Syndrome (AIDS), and the rest of the world followed.

  Naming the syndrome was the least of the early challenges. More urgent was to identify its cause. No one knew, back when those reports from Gottlieb and Friedman-Kien began capturing attention, what sort of pathogen caused this combination of puzzling, lethal symptoms—nor even if there was a single pathogen. The virus idea arose, after other mistaken hypotheses, as a plausible guess.