The Chimp and the River: How AIDS Emerged from an African Forest (2 page)

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, Gaëtan 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

I
n 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.

One scientist who made the guess was Luc Montagnier, then a little-known molecular biologist at the Institut Pasteur in Paris. Montagnier’s research focused mainly on cancer-causing viruses, especially the group known as retroviruses, some of which cause tumors in birds and mammals. Retroviruses are fiendish things, even more devious and persistent than the average virus. They take their name from the capacity to move backward (retro) against the usual expectations of how a creature translates its genes into working proteins. Instead of using RNA as a template for translating DNA into proteins—the usual route by which genetic information becomes living reality—a retrovirus converts its RNA into DNA within a host cell; its viral DNA then penetrates the cell nucleus and gets itself integrated into the genome of the host cell, thereby guaranteeing replication of the virus whenever the host cell reproduces itself. Luc Montagnier had studied these things in animals—chickens, mice, primates—and wondered about the possibility of finding them in human tumors too. Another disquieting possibility about retroviruses was that the new disease showing up in America and Europe, AIDS, might be caused by one.

There was still no solid proof that it was caused by a virus of any sort. But three kinds of evidence pointed that way, and Montagnier recalled them in his memoir, a book titled
Virus
. First, the incidence of AIDS among homosexuals linked by sexual interactions suggested that this was an infectious disease. Second, the incidence among intravenous drug users suggested a blood-borne infectious agent. Third, the cases among hemophiliacs implied a blood-borne agent that escaped detection in processed blood products such as clotting factor. So: It was contagious, blood-borne, infinitesimal. “AIDS
could not be caused by a conventional bacterium, a fungus, or protozoan,” Montagnier wrote, “since these kinds of germs are blocked by the filters through which the blood products necessary to the survival of hemophiliacs are passed. That left only a smaller organism: the agent responsible for AIDS thus could only be a virus.”

Other evidence hinted that, among all viral possibilities, it might be a retrovirus. This was new ground, but then so was AIDS. The only known human retrovirus as of early 1981 was something called human T-cell leukemia virus (HTLV), recently discovered under the leadership of a smart, outgoing, highly regarded, and highly ambitious researcher named Robert Gallo, whose Laboratory of Tumor Cell Biology was part of the National Cancer Institute in Bethesda, Maryland. HTLV, as its name implies, attacks T cells and can turn them cancerous. T cells are one of the three major types of lymphocyte of the immune system. (Later the acronym HTLV was recast to mean human T-lymphotropic virus, which is slightly more accurate.) A related retrovirus, feline leukemia virus, causes immunodeficiency in cats. So a suspicion arose among cancer-virus researchers that the AIDS agent, destroying human immune systems by attacking their lymphocytes (in particular, a subcategory of T cells known as T-helper cells), might likewise be a retrovirus. Montagnier’s group began looking for it.

Gallo’s lab did too. And those two weren’t alone. Other scientists at other laboratories around the world recognized that finding the cause of AIDS was the hottest, the most urgent, and potentially the most rewarding quest in medical research. By late spring of 1983, three teams working independently had each isolated a candidate virus, and in the May 20 issue of
Science
, two of those teams published announcements. Montagnier’s group in Paris, screening cells from a thirty-three-year-old
homosexual man suffering from lymphadenopathy (swollen lymph nodes), had found a new retrovirus, which they called LAV (for lymphadenopathy virus). Gallo’s group came up with a new virus also, one that Gallo took for a close relative of the human T-cell leukemia viruses (by now there was a second, called HTLV-II, and the first had become HTLV-I) that he and his people had discovered. He called this newest bug HTLV-III, nesting it proprietarily into his menagerie. The French LAV and the Gallo HTLVs had at least one thing in common: They were indeed retroviruses. But within that family exists some rich and important diversity. An editorial in the same issue of
Science
trumpeted the Gallo and Montagnier papers with a misleading headline:
HUMAN T-CELL LEUKEMIA VIRUS LINKED TO AIDS,
despite the fact that Montagnier’s LAV was
not
a human T-cell leukemia virus. Woops, mistaken identity. Montagnier knew better, but his
Science
paper seemed to blur the distinction, and the editorial occluded it entirely.

Then again, neither was Gallo’s “HTLV-III” an HTLV, once it was clearly seen and correctly classified. It turned out to be something nearly identical to Montagnier’s LAV, of which Montagnier had given him a frozen sample. Montagnier had personally delivered that sample, carrying it on dry ice during a visit to Bethesda.

Confusion was thus sown early—confusion about what exactly had been discovered, who had discovered it, and when. That confusion, irrigated with competitive zeal, fertilized with accusation and denial, would grow rife for decades. There would be lawsuits. There would be fights over royalties from the patent on an AIDS blood-screening test that derived from virus grown in Gallo’s lab but traceable to Montagnier’s original isolate. (Contamination from one experiment to another, or from one batch of samples to another, is a familiar problem in lab work with viruses.) It wasn’t a petty squabble. It was a big squabble,
in which pettiness played no small part. What was ultimately at stake, besides money and ego and national pride, was not just advancing or retarding research toward an AIDS cure or vaccine but also the Nobel Prize in medicine, which eventually went to Luc Montagnier and his chief collaborator, Françoise Barré-Sinoussi.

Meanwhile the third team of researchers, led quietly by a man named Jay A. Levy in his lab at the University of California School of Medicine, in San Francisco, also found a candidate virus in 1983 but didn’t publish until more than a year afterward. By summer of 1984, Levy noted, AIDS had affected “more than 4000 individuals in the world; in San Francisco, over 600 cases have been reported.” Those numbers sounded alarmingly high at the time, though in retrospect, compared with 36 million deaths, they seem poignantly low. Levy’s discovery was also a retrovirus. His group detected it in twenty-two AIDS patients and grew more than a half dozen isolates. Because the bug was an AIDS-associated retrovirus, Levy called it ARV. He suspected, correctly, that his ARV and Montagnier’s LAV were simply variant samples of the same evolving virus. They were very similar but not
too
similar. “Our data cannot reflect a contamination of our cultures with LAV,” he wrote, “since the original French isolate was never received in our laboratory.” Harmless as that may sound, it was an implicit jab at Robert Gallo.

The details of this story, the near-simultaneous triple discovery and its aftermath, are intricate and contentious and seamy and technical, like a ratatouille of molecular biology and personal politics left out in the sun to ferment. They lead far afield from the subject of zoonotic disease. For our purposes here, the essential point is that a virus discovered in the early 1980s,
in three different places under three different names, became persuasively implicated as the causal agent of AIDS. A distinguished committee of retrovirologists settled the naming issue in 1986. They decreed that the virus would be called HIV.

3

I
t’s quite appropriate and more than coincidental, given the zoonotic dimension of this story, that the next phase began with a veterinarian. Max Essex studied retroviruses in monkeys and cats.

Dr. Myron (Max) Essex, DVM, PhD, was not your ordinary small-animal vet. He was a professor and a research scientist in the Department of Cancer Biology at the Harvard School of Public Health. He had worked on feline leukemia virus (FeLV), among other things, and cancer-causing viruses formed the broad frame of his interests. Having seen the effects of FeLV in wrecking the immune systems of cats, he suspected as early as 1982, along with Gallo and Montagnier, that the new human immune deficiency syndrome might be caused by a retrovirus.

Then something strange came to his notice, by way of a grad student named Phyllis Kanki. She was a veterinarian like him, but now working on a doctorate there at the School of Public Health. Kanki grew up in Chicago, spent her adolescent summers doing zoo work, then studied biology and chemistry on the way toward veterinary medicine and comparative pathology. During the summer of 1980, while still amid her DVM studies, she worked at the New England Regional Primate Research
Center, which was part of Harvard but located out in Southborough, Massachusetts. There she saw a weird problem among the center’s captive Asian macaques—some of them were dying of a mysterious immune dysfunction. A macaque is a kind of monkey, and several of the Asian species, such as the rhesus macaque and the Formosan rock macaque, are highly valued as laboratory animals for medical research. At the primate center, which held almost eight hundred animals of the macaque genus, Formosan rock macaques in particular seemed to be suffering this immune-system failure. Their T-helper lymphocyte counts were way down. They wasted away from diarrhea or succumbed to opportunistic infections, including
Pneumocystis carinii.
It sounded too much like AIDS. Kanki later brought this to the attention of Essex, her thesis adviser, and together with colleagues from Southborough, they started to look for what was killing those monkeys. Based on their knowledge of FeLV and other factors, they wondered whether it might be a retrovirus infection.