the Half-Portuguese Merchant, the Tall Boy, the Crocodile, and the Blue-Eyed Bobangi. In his telling, the Tall Boy became an adult and the Crocodile was very large, a leviathan. No one doubted his word. They knew he had come down the river and it must have been perilous. The crocodile skull wasn’t there to belie him. During those years he slept with thirteen women, all of whom were femmes libres to one degree or another. One of those, a young Tio girl who had recently arrived in Brazzaville from upriver, and who found that she fancied him more than she did her freedom, became his wife. Eventually he infected her with the virus. He also infected one other, a rather more professional woman who lived in a small house in the Bacongo neighborhood, west of town, where he visited her on an intermittent basis when his wife was pregnant. The other eleven women had only fleeting sexual contacts with him and were luckier. They remained HIV-negative. The Voyager’s personal lifetime R0 was therefore precisely 2.0. People liked him and were sorry when he fell ill.
The Bacongo girlfriend was vivacious and pretty and ambitious for wider horizons, so she crossed the pool to Léopoldville, where she had a successful career, though not a long one.
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If the virus reached Léopoldville in 1920 or so, that still leaves a gap of four decades to the time of ZR59 and DRC60, those earliest archival HIV sequences. What happened during the interim? We don’t know, but available evidence allows a rough sketch of the outlines of possibility.
The virus lurked in the city. It replicated within individuals. It passed from one person to another by sexual contact, and possibly also by the reuse of needles and syringes for treatment of well-known diseases such as trypanosomiasis. (More on that possibility, below.) Whatever its means of transmission, presumably HIV caused immune deficiency, eventually death, among most or all people infected—except those who died early from other causes. But it didn’t yet assert itself conspicuously enough to be recognized as a distinct new phenomenon.
It may also have proliferated slowly in Brazzaville, across the pool, helped along there too by changing sexual mores and programs of therapeutic injection. It may have lingered in villages of southeastern Cameroon or elsewhere in the upper Sangha basin.
And wherever it was, but definitely in Léopoldville, it continued to mutate. The wide divergence between ZR59 and DRC60 tells us that. It continued to evolve.
Studying the evolutionary history of HIV-1 is more than an idle exercise. The point is to understand how one strain of the virus (group M) made itself so deadly and widespread among humans. Such understanding, in turn, may lead toward better measures to control the devastation of AIDS, possibly by way of a vaccine, more likely by way of improved treatments. That’s why scientists such as Beatrice Hahn, Michael Worobey, and their colleagues explore the molecular phylogenetics of HIV-1, HIV-2, and the various SIVs. One issue they address is whether the virus became virulent before, or only after, its spillover from chimpanzees. To state the question more plainly: Does SIVcpz kill chimps, or is it only an innocuous passenger? Answering that one could reveal something important about how human bodies respond to HIV-1.
For a while after the discovery of SIVcpz, the prevailing impression was that it’s harmless in chimpanzees, an ancient infection that may once have caused symptoms but no longer does. This impression was bolstered by the fact that, in the earlier years of AIDS research, more than a hundred captive chimpanzees were experimentally infected with HIV-1 and none showed immune system failure. When a single lab chimpanzee did progress to AIDS (ten years after experimental infection with three different strains of HIV-1), its case was remarkable enough to merit a six-page paper in the Journal of Virology. The researchers implied that this was good news, finally offering hope that chimpanzees do represent a relevant experimental model (that is, a sufficiently analogous test subject) for studying human AIDS. There was even a report, based on genetic analysis of captive animals in the Netherlands, suggesting that chimpanzees had “survived their own AIDS-like pandemic” more than 2 million years ago. They emerged from the experience, according to this line of thought, with genetic adaptations that render them resistant to the effects of the virus. They still carry it but apparently don’t get sick. That notion, to repeat, was founded on captive chimpanzees. As for SIV-positive chimps in the wild, no one knew whether