SARS pg. 4
Even if the civet is confirmed to be the culprit in transmitting the SARS coronavirus to human beings, eliminating contact with the animal will only go so far to prevent future outbreaks. The potential will still exist for animal coronaviruses—and other classes of viruses as well—to jump from animals to human beings.
RNA viruses, with their propensity for mutation, are especially likely to cause emerging infectious diseases, Denison says. The polymerase enzyme that copies the coronavirus genome, for example, has a high error rate—it makes lots of mistakes, resulting in virus particles with mutations. Some of these random changes may result in dead viruses, others may have no effect, and still others may make the virus better at infecting another species.
“Viruses don’t ‘respond’ to things like antiviral drugs, antibodies, temperature … they’re making changes all the time,” Denison explains. “Viruses are incredibly adaptive.
“I like to picture a kind of ‘king of the hill’ model,” he says. “You’ve got the dominant viral population at the top, and all the time these other viruses are being produced. It’s like a coup d’etat-in-waiting -- if circumstances change, there’s another virus group there ready to depose the king.”
A study published this winter in the journal Science demonstrates just how adaptive the SARS coronavirus proved to be. A consortium of Chinese scientists tracked the virus’ evolution—the changes in its genetic code—during last year’s epidemic by analyzing the viral genome in tissue samples from patients infected during the early, middle and late phases of the epidemic.