Spillover: Animal Infections and the Next Human Pandemic by David Quammen Page A

those, tested posthumously, were negative.) Ten employees who had helped unload and handle the monkeys were also screened for infection, and they also tested negative, but none of them were euthanized.
    Uganda became the next known locus of the virus in Africa, with an outbreak of Sudan virus that began near the northern town of Gulu in August 2000. Northern Uganda shares a border with what in those days was southern Sudan, and it wasn’t surprising that Sudan virus might cross or straddle that border. Cross it how, straddle it how? By way of the individual movements or the collective distribution of the reservoir species, identity unknown. This is a pointed example of why solving the reservoir mystery is important: If you know which animal harbors a certain virus and where that animal lives—and conversely, where it doesn’t live—you know where the virus may next spill over, and where it probably won’t. That provides some basis for focusing your vigilance. If the reservoir is a rodent that lives in the forests of southwestern Sudan but not in the deserts of Niger, the goat herders of Niger can relax. They have other things to worry about.
    In Uganda, unfortunately, the 2000 spillover led to an epidemic of Sudan virus infections that spread from village to village, from hospital to hospital, from the north of the country to the southwest, killing 224 people.
    The case fatality rate was again “only” 53 percent, exactly what it had been in the first Sudanese outbreak, back in 1976. This precise coincidence seems to reflect a significant difference in virulence between Sudan and Ebola viruses. Their difference, in turn, might reflect different evolutionary adjustments to humans as a secondary host (though random happenstance is also a possible explanation). Many factors contribute to the case fatality rate during an outbreak, including diet, economic conditions, public health in general, and the medical care available in the location where an outbreak occurs. It’s hard to isolate the inherent ferocity of a virus from those contextual factors. What can be said, though, is that Ebola virus appears to be the meanest of the four ebolaviruses you’ve heard about, as gauged by its effect on human populations. Taï Forest virus can’t reliably be placed on that spectrum at all, not yet—for lack of evidence. Having infected just one known human (or possibly two, counting an unconfirmed later case) and killed none, Taï Forest virus may be less prone to spillover. It may or may not be less lethal; one case, like one roll of the dice, proves nothing about what’s likely to emerge as numbers grow larger. Then again, Taï Forest virus might also be spilling more frequently but inconsequentially—infecting people yet not causing notable illness. No one has screened the populace of Côte d’Ivoire to exclude that possibility.
    The role of evolution in making Taï Forest virus (or any virus) less virulent in humans is a complicated matter, not easily deduced from simple comparison of case fatality rates. Sheer lethality may be irrelevant to the virus’s reproductive success and long-term survival, the measures by which evolution keeps score. Remember, the human body isn’t the primary habitat of ebolaviruses. The reservoir host is.
    Like other zoonotic viruses, ebolaviruses have probably adapted to living tranquilly within their reservoir (or reservoirs), replicating steadily but not abundantly and causing little or no trouble. Spilling over into humans, they encounter a new environment, a new set of circumstances, often causing fatal devastation. And one human can infect another, through direct contact with bodily fluids or other sources of virus. But the chain of ebolavirus infection, at least so far, has never continued through many successive cases, great distances, or long stretches of time. Some scientists use the term “dead-end host,” as distinct from “reservoir host,” to describe humanity’s role in the