The evolution of viral emergence

The current uncertainty over whether H5N1 avian influenza virus will successfully adapt to human transmission highlights the importance of understanding the evolutionary basis of viral emergence, particularly the respective roles played by ecology and genetics in allowing viruses to establish productive transmission networks in new host species. Work by Anishchenko et al. (1) in this issue of PNAS reveals that even small changes in viral genomes can have a fundamental impact on fitness in new hosts, therein facilitating disease emergence.

Although RNA viruses are often able to adapt to changing environments with remarkable rapidity, an adaptability that stems from their high mutation rates and large population sizes (2), it is also the case that the evolution of ongoing transmission in new host species is rather harder to achieve. Indeed, of the many RNA viruses that are categorized as “emerging,” the great majority is in reality “spillover” infections with little or no subsequent transmission. The transmission of avian H5N1 virus in humans is a perfect case in point; despite numerous avian-to-human spillover infections, to date there is no compelling evidence of secondary, sustained human-to-human transmission, the crucial step in establishing a full-blown epidemic. This pattern of repeated exposure without large-scale transmission seems particularly typical of arthropod-borne RNA viruses (“arboviruses”), which are a common cause of spillover infections but rarely fully adapt to new host transmission cycles. The answer to this apparent paradox (why rapidly evolving RNA viruses often have trouble in achieving what might appear to be simple adaptive solutions) is that adaptation to new hosts is often polygenic, involving multiple mutations in a variety of genes and which may exhibit complex fitness tradeoffs. In population genetic terms, a virus has to move from one fitness peak (successful transmission in the reservoir host …

*E-mail: ech15{at}psu.edu