Free The Viral Storm by Nathan Wolfe

infecting them, which in turn contributed to lower microbial repertoires for our ancestors.
    The kinds of animals living in the savanna also differed in critical ways from those in the forests, including a marked contrast in the diversity of apes and other primates. Simply put—primates love forests. The king of the jungle is a primate, not a lion. While some primates, like baboons and vervet monkeys, live very successfully in savanna habitats, forest regions trump savanna regions in terms of primate diversity. When we consider the microbes that could most easily infect our ancestors, the diversity of primates in any given habitat plays an important role. They are certainly not the only species that contribute to our microbial repertoires—in my own studies, I focus not only on primates but also on bats and rodents—but they do play an important role.
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    Some years ago, I began considering what factors might improve or decrease the chances that a microbe would jump from one host to the next successfully enough to catch on and spread in the new host. It may seem that bats and snakes, for example, would provide similar sources for novel microbes. Yet there is a strong argument against this idea. Long evident to those doing work on microbes in laboratories is the fact that closely related animals have similar susceptibility to certain infectious agents. So a mammal, like a bat, would have many more microbes that could be successfully shared with a human than a snake. If not for the logistics and ethics, chimpanzees would make the ideal models for studying just about every human infectious disease. As our closest living relatives, they have nearly identical susceptibility to the microbes that infect us. Over time, less and less laboratory research on human microbes is conducted in chimpanzees, but this is largely because of the valid ethical concerns associated with conducting research on them and the difficulty of controlling these large and aggressive animals in captivity.
    Closely related animal species will share similar immune systems, physiologies, cell types, and behaviors, making them vulnerable to the same groups of infectious agents. In fact, the taxonomic barriers that we place on species are constructs of our own scientific systems, not nature. Viruses don’t read field guides. If two different hosts share sufficiently similar bodies and immune systems, the bug will move between them irrespective of how a museum curator would separate them. I named this concept the academically accurate but unwieldy taxonomic transmission rule , and it holds up for chimpanzees and humans as it would for dogs and wolves. 1 The idea is that the more closely related any two species are, the higher the probability that a microbe can successfully jump between them.
    Most of the major diseases of humans originated at some point in animals, something I analyzed in a paper for Nature , written with colleagues in 2007. We found that among those for which we can easily trace an animal origin, virtually all came from warm-blooded vertebrates, primarily from our own group, the mammals, which includes the primary subjects of my own research, the primates, bats, and rodents. In the case of primates, while they constitute only 0.5 percent of all vertebrate species, they seeded nearly 20 percent of major infectious diseases in humans. When we divided the number of animal species in each of the following groups by the number of major human diseases they contributed, we obtained a ratio that expresses the importance of each group for seeding human disease. The numbers are striking: 0.2 for apes, 0.017 for the other nonhuman primates, 0.003 for mammals other than primates, and a number approaching 0 for animals other than vertebrates. So as our early ancestors left the primate-packed rain forests and spent more time with lower overall primate biodiversity in savanna habitats, they moved into regions that likely had a lower diversity of