but slightly ambiguous. Antibody testing is an indirect gauge of infection, relatively convenient and quick, but imprecise. Greater precision comes with detecting fragments of viral RNA or, better still, isolating a virus—catching the thing in its wholeness and growing it in quantity—from which a confident identification can be made. Martine Peeters and her co-workers succeeded in isolating a virus from the baby chimp. Twenty years later, when I called on her at her office at an institute in southern France, Peeters remembered vividly how that virus showed up in a series of molecular tests.
“It was especially surprising,” she said, “because it was so close to HIV-1.”
Had there been any previous hints?
“Yes. At that time we knew already that HIV-2 most likely came from primates in West Africa,” she said, alluding to the sooty mangabey work. “But there was no virus close to HIV-1 already detected in primates. And until now, it’s still the only virus close to HIV-1.” Her group had published a paper, in 1989, announcing the new virus and calling it SIVcpz. They did not crow about having found the reservoir of HIV-1. Their conclusion from the data was more modest: “It has been suggested that human AIDS retroviruses originated from monkeys in Africa. However, this study and other previous studies on SIV do not support this suggestion.” Left implicit: Chimpanzees, not monkeys, might be the source of the pandemic bug.
By the time I met her, Martine Peeters was director of research at the Institut de Recherche pour le Développement, in Montpellier, a handsome old city just off the Mediterranean coast. She was a small, blonde woman in a black sweater and silver necklace, concise and judicious in conversation. What sort of response had met this discovery? I asked.
“HIV-2, people accepted it readily.” They accepted, she meant, the notion of simian origins. “But HIV-1, people had more difficulties to accept it.”
Why the resistance? “I don’t know why,” she said. “Maybe because we were young scientists.”
The 1989 paper got little attention, which seems peculiar in retrospect, given the novelty and gravity of what it implied. In 1992 Peeters published another, describing a third case of SIVcpz, this one in a captive chimpanzee that had been shipped to Brussels from Zaire. All three of her SIV-positive results had been in “wild-born” chimpanzees taken captive (as distinct from animals bred in captivity) but that still left a gap in the chain of evidence. What about chimps still in the wild?
With only such tools of molecular biology as available in the early 1990s, the screening of wild chimps was difficult (and unacceptable to most chimp researchers), because the diagnostic tests required blood sampling. Lack of evidence from wild populations, in turn, contributed to skepticism in the AIDS-research community about the link between HIV-1 and chimps. After all, if Asian macaques had become infected with HIV-2 in their cages, from contact with African monkeys, might not SIV-positive chimpanzees simply reflect cage-contact infections too? Another reason for skepticism was the fact that, by the end of the 1990s, roughly a thousand captive chimpanzees had been tested but, apart from Peeters’s three, not a single one had yielded traces of SIVcpz. These two factors—the absence of evidence from wild populations and the extreme rarity of SIV in captive chimps—left open the possibility that both HIV-1 and SIVcpz derived directly from a common ancestral virus in some other primate. In other words, maybe those three lonely chimps had gotten their infections from some still-unidentified monkey, and maybe the same unidentified monkey had given HIV-1 to humans. With that possibility dangling, the origin of HIV-1 remained uncertain for much of the decade.
In the meantime, researchers investigated not just the source of HIV but also its diversity in humans, discovering three major lineages of HIV-1. “Groups” became the preferred term for these lineages. Each group was a cluster of strains that was genetically discrete from the other clusters; there was variation within each group, since HIV is always evolving, but the differences between groups were far larger. This pattern of groups had some dark implications that dawned on scientists only gradually and still haven’t been absorbed in the popular understanding of AIDS. I’ll get to them shortly, but first let’s consider the pattern itself.
Group M was the most widespread and nefarious. The letter M stood for “main,” because that group accounted for most of the HIV infections worldwide. Without HIV-1 group M, there was no global pandemic, no millions of deaths. Group O was the second to be