The Chimp and the River: How AIDS Emerged from an African Forest Read Online Free PDF

origination on sooty mangabeys, “and evolved as SIV mac and HIV-2, respectively.” In fact, those three strains were very similar, suggesting divergence fairly recently from a common ancestor.
    “A plausible interpretation of these data,” Hirsch and her coauthors added, to make the point plainly, “is that in the past 30–40years SIV from a West African sooty mangabey (or closely related species) successfully infected a human and evolved as HIV-2.” It was official: HIV-2 is a zoonosis.

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    B ut what about HIV-1? Where did the great killer come from? That was a larger mystery that took somewhat longer to solve. The logical inference was that HIV-1 must be zoonotic in origin also. But what animal was its reservoir? When, where, and how had spillover occurred? Why had the consequences been so much more dire?
    HIV-2 is both less transmissible and less virulent than HIV-1. The molecular bases for those fateful differences are still secrets embedded in the genomes, but the ecological and medical ramifications are clear and stark. HIV-2 is confined mostly to West African countries such as Senegal and Guinea-Bissau (the latter of which, during colonial times, was Portuguese Guinea), and to other areas connected socially and economically within the former Portuguese empire, including Portugal itself and southwestern India. People infected with HIV-2 tend to carry lower levels of virus in their blood, to infect fewer of their sexual contacts, and to suffer less severe or longer-delayed forms of immunodeficiency. Many of them don’t seem to progress to AIDS at all. And mothers who carry HIV-2 are less likely to pass it to their infants. The virus is bad, but not nearly so bad as it could be. HIV-1 provides the comparison. HIV-1 is the thing that afflicts tens of millions of people throughout the world. HIV-1 is the pandemic scourge. Tounderstand how the AIDS catastrophe has happened to humanity, scientists had to trace HIV-1 to its source.
    This takes us to the city of Franceville, in southeastern Gabon, Central Africa, and an institution called the Centre International de Recherches Médicales (CIRMF), the same place at which important work on Ebola virus has been done. It’s a nexus for the study of, and response to, emerging African diseases. At the end of the 1980s, a young Belgian woman named Martine Peeters worked as a research assistant at CIRMF for a year or so, during the period between getting her diploma in tropical medicine and going on for a doctorate. The CIRMF facility maintained a compound of captive primates, including three dozen chimpanzees, and Peeters along with several associates was tasked with testing the captive animals for antibodies to HIV-1 and HIV-2. Almost all of the chimps tested negative—all except two. Both exceptions were very young females, recently captured from the wild. Such baby chimps, like other orphan primates, are sometimes kept or sold off as pets after the killing and eating of their mothers. One of these animals, a two-year-old suffering from gunshot wounds, had been brought to CIRMF for medical treatment. She died of the wounds, but not before surrendering a blood sample. The other was an infant, maybe six months old, who survived. Blood serum from each of them reacted strongly when tested against HIV-1, less strongly when tested against HIV-2. That much was notable 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 southernFrance, Peeters remembered vividly how that virus showed up in a series of molecular tests.
    “It was especially