David Quammen

measures them, roundish viruses range from around fifteen nanometers (that’s fifteen billionths of a meter) in diameter to around three hundred nanometers. But viruses aren’t all roundish. Some are cylindrical, some are stringy, some look like bad futuristic buildings or lunar landing modules. Whatever the shape, the interior volume is minuscule. The genomes packed within such small containers are correspondingly limited, ranging from 2,000 nucleotides up to about 1.2 million. The genome of a mouse, by con

The capsid shouldn’t be mistaken for a cell wall or a cell membrane. It’s merely analogous. Viruses, from the beginning of virology, have been defined in the negative (not captured by a filter, not cultivable in chemical nutrients, not quite alive), and the most fundamental negative axiom is that a virion is not a

so important I’ll repeat it: RNA viruses mutate profligately.
Mutation supplies new genetic variation. Variation is the raw material upon which natural selection operates. Most mutations are harmful, causing crucial dysfunctions and bringing the mutant forms to an evolutionary dead end. But occasionally a mutation happens to be useful and adaptive. And the more mutations occurring, the greater chance that good ones will turn up. (More mutations also

Viruses face four basic challenges: how to get from one host to another, how to penetrate a cell within that host, how to commandeer the cell’s equipment and resources for producing multiple copies of itself, and how to get back out—out of the cell, out of the host, on to the next. A virus’s structure and genetic capabilities are shaped parsimoniously to those tasks.

corrective arrangement, no such buddy-buddy system, no such proofreading polymerase, sustain rates of mutation that may be thousands of times higher. (For the record, there’s also a smaller group of DNA viruses that code their genetics on single strands of DNA and suffer high mutation rates, as in RNA. And there’s a little group of double-stranded RNA viruses. To every rule, an exception. But we’re going to ignore those minor anomalies because this stuff is already complicated enough.) The basic point is

replication. Viruses, lacking cell walls, lacking internal metabolic processes, are oblivious to the effects of such killer drugs.
Inside the viral capsid is usually nothing but genetic material, the set of instructions for creating new virions on the same pattern. Those instructions can only be implemented when they’re inserted into the works of a living cell. The material itself may be either DNA or RNA, depending on the family of virus. Both types of molecule are capable of recording and expressing information,

hantaviruses, all the influenzas, and the common cold viruses, store their genetic information in the form of RNA.
The different attributes of DNA and RNA account for one of the most crucial differences among viruses: rate of mutation. DNA is a double-stranded molecule, the famed double helix, and because its two strands fit together by way of those very specific relationships between pairs of nucleotide bases (adenine linking only with thymine, cytosine only with guanine), it generally re

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.

National Foundation for Infantile Paralysis (aka the March of Dimes) consumed seventeen thousand monkeys. The foundation maintained a sort of clearinghouse for imported monkeys in South Carolina, from which one leading researcher had a standing order of fifty macaques per month, at $26 apiece, delivered. Nobody knows exactly how many macaques were “sacrificed” in the labs of Albert Sabin and Jonas Salk, let alone other researchers, but the incidence of herpes B infections peaked in 1957–