genes from the host, which helps them to confuse a host’s immune response. They can reside in a body for longer stretches of time, content to get themselves passed along by slower modes of transmission, such as sexual and vertical. Most crucially, they can repair copying errors as they replicate, thus lowering their mutation rates. “RNA viruses can’t do that.” They face a different set of limits and options. Their mutation rates can’t be lowered. Their genomes can’t be enlarged. “They’re kind of stuck.”
What do you do if you’re a virus that’s stuck, with no long-term security, no time to waste, nothing to lose, and a high capacity for adapting to new circumstances? By now we had worked our way around to the point that interested me most. “They jump species a lot,” Eddie said.
VII
CELESTIAL HOSTS
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From where do these viruses jump? They jump from animals in which they have long abided, found safety, and occasionally gotten stuck. They jump, that is, from their reservoir hosts.
And which animals are those? Some kinds are more deeply implicated than others as reservoirs of the zoonotic viruses that jump into humans. Hantaviruses jump from rodents. Lassa too jumps from rodents. Yellow fever virus jumps from monkeys. Monkeypox, despite its name, seems to jump mainly from squirrels. Herpes B jumps from macaques. The influenzas jump from wild birds into domestic poultry and then into people, sometimes after a transformative stopover in pigs. Measles may originally have jumped into us from domesticated sheep and goats. HIV-1 has jumped our way from chimpanzees. So there’s a certain diversity of origins. But a large fraction of all the scary new viruses I’ve mentioned so far, as well as others I haven’t mentioned, come jumping at us from bats.
Hendra: from bats. Marburg: from bats. SARS-CoV: from bats. Rabies, when it jumps into people, comes usually from domestic dogs—because mad dogs get more opportunities than mad wildlife to sink their teeth into humans—but bats are among its chief reservoirs. Duvenhage, a rabies cousin, jumps to humans from bats. Kyasanur Forest virus is vectored by ticks, which carry it to people from several kinds of wildlife, including bats. Ebola, very possibly: from bats. Menangle: from bats. Tioman: from bats. Melaka: from bats. Australian bat lyssavirus, it may not surprise you to learn, has its reservoir in Australian bats. And though the list already is long, a little bit menacing, and in need of calm explanation, it wouldn’t be complete without adding Nipah, one of the more dramatic RNA viruses to emerge within recent decades, which leaps into pigs and via them into humans: from bats.
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The debut appearance of a new zoonotic disease is often confusing as well as alarming, and Nipah was no exception. In September 1998, people began getting sick in a northern district of peninsular Malaysia, near the city of Ipoh. Their symptoms included fever, headache, drowsiness, and convulsions. The victims were pig farmers or somehow associated with pig processing. One was a pork seller, who died of a brain inflammation. In December, after the northern outbreak seemed to be tapering off, a new cluster of cases appeared southwest of the capital, Kuala Lumpur, in a pig-farming area of the state of Negri Sembilan. By the end of the year, ten workers had fallen ill, gone comatose, and died. The government reacted quickly but with imperfect comprehension. At first it was all about mosquitoes and pigs.
Mosquitoes were implicated as the presumed vectors; pigs, as the presumed reservoir hosts. But vectors and reservoirs of what? Japanese encephalitis virus was the presumed cause.
Japanese encephalitis (JE) is an endemic disease in Malaysia and much of southeastern Asia, tallying upward of thirty thousand human cases (mostly nonfatal) throughout the region each year. The JE virus belongs to the same family as West Nile, dengue, and yellow fever virus. It’s vector-borne, traveling by mosquito from its reservoirs in domestic pigs and wild birds. Antibodies found in some of the sickened Malaysian pig workers seemed to confirm its responsibility for the 1998 outbreak, and so Japanese encephalitis became the object of rising public concern and government action. Health officials started pondering how many people—or how many pigs—they should vaccinate against it.
In early January, a story ran in the New Straits Times, Malaysia’s leading English-language newspaper, under the headline: GIRL IS FOURTH PERSON IN NEGRI TO DIE OF ENCEPHALITIS. The girl in question, thirteen years old and unnamed in the article, had been helping her family with their pig business. Below the piece about her was