Spillover - By David Quammen Page 0,174

blue curtain, that sample and hundreds of others had traveled a circuitous route, to Belgium and then the United States, ending up in the laboratory of a young biologist at the University of Arizona. Michael Worobey is a Canadian, originally from British Columbia, whose specialty is molecular phylogenetics. After his undergraduate work he went to Oxford on a Rhodes scholarship, which ordinarily means two years of mildly strenuous academic work plus lots of tea, sherry, tennis on grass, and genteel anglophilia before the “scholar” returns to professional school or a career. Worobey put Oxford to more serious use, staying on, finishing a doctorate and then a postdoc fellowship in evolutionary biology at the molecular level. From there he returned to North America in 2003, accepting an assistant professorship at Arizona and building himself a BSL-3 lab for work on the genomes of dangerous viruses. Several years later, it was Worobey who detected evidence of HIV in a certain Congolese biopsy specimen from 1960.

Worobey amplified fragments of the viral genome, pieced the fragments together, recognized them as an early version of HIV-1, and named the sequence DRC60. Comparing his sequence with ZR59, the other earliest known strain, he reached a dramatic conclusion: that the AIDS virus has been present in humans for decades longer than anyone thought. The pandemic may have gotten its start with a spillover as early as 1908.

To appreciate Worobey’s discovery and how it splashed down amid previous ideas, you’ll need to know a little context. That context involved a heated dispute over just how HIV-1 entered the human population. The prevailing notion as of the early 1990s, based on what had been learned about HIV-2 and the sooty mangabey, among other factors, was that HIV-1 also came from an African primate, and that it had probably gotten into humans by way of two separate instances (for groups M and O, the ones then recognized) of butchering bushmeat. This became known as the cut-hunter hypothesis. In each instance, a man or a woman had presumably butchered the carcass of an SIV-positive primate and suffered exposure through an open wound—maybe a cut on the hand, or a scratch on the arm, or a raw spot on any skin surface that got smeared with the animal’s blood. A wound on the back might have sufficed, if the carcass were draped over shoulders for carrying home. A wound in the mouth, if some of the meat were consumed raw. All that mattered was blood-to-blood contact. The cut-hunter hypothesis was speculative but plausible. It was parsimonious, requiring few complications and no unlikelihoods. It fit the known facts, though the known facts were fragmentary. And then in 1992 a contrary theory arose.

This one was heterodox and highly controversial: that HIV-1 first got into humans by way of a contaminated polio vaccine tested on a million unsuspecting Africans. The vaccine itself, by this theory, had been an unintended delivery system for AIDS. Someone, according to the theory, had monumentally goofed. Someone was culpable. Scientific hubris had overridden caution, with catastrophic results. The scariest thing about the polio-vaccine theory was that it also seemed plausible.

Viruses are subtle, as you’ve seen. They get in where they shouldn’t. Laboratory contaminations occur. Even viral or bacterial contamination of a vaccine at the production level—it has happened. Back in 1861, a group of Italian children vaccinated against smallpox, with material direct from a “vaccinal sore,” came down with syphilis. Smallpox vaccine administered to kids in Camden, New Jersey, at the start of the twentieth century, seems to have been contaminated with tetanus bacillus, resulting in the death of nine vaccinated children from tetanus. Around the same time, a batch of diphtheria antitoxin prepared in St. Louis, using blood serum from a horse, also turned out to carry tetanus, which killed another seven children. Producers then began filtering vaccines, an effective precaution against bacterial contamination; but viruses passed through the filters. Formaldehyde was sometimes added to inactivate a target virus, and that supposedly killed unwanted viruses too, but the supposition wasn’t always correct. As late as midcentury, some of the early batches of the Salk polio vaccine were contaminated with a virus known as SV40, endemic in rhesus macaques. SV40 in vaccine became a hot issue, several years later, when suspicions arose that this virus causes cancer.

Whether vaccine contamination happened with HIV-1, and far more consequentially, is another matter. That the vaccine in question had been given to Africans was not in dispute. Between 1957 and 1960, a Polish-born American

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