Abstract
Due to error-prone replication, RNA viruses exist within hosts as a heterogeneous population of non-identical, but related viral variants. These populations may undergo bottlenecks during transmission that stochastically reduce variability leading to fitness declines. Such bottlenecks have been documented for several single-host RNA viruses, but their role in the population biology of obligate two-host viruses such as arthropod-borne viruses (arboviruses) in vivo is unclear, but of central importance in understanding arbovirus persistence and emergence. Therefore, we tracked the composition of West Nile virus (WNV; Flaviviridae, Flavivirus) populations during infection of the vector mosquito, Culex pipiens quinquefasciatus to determine whether WNV populations undergo bottlenecks during transmission by this host. Quantitative, qualitative and phylogenetic analyses of WNV sequences in mosquito midguts, hemolymph and saliva failed to document reductions in genetic diversity during mosquito infection. Further, migration analysis of individual viral variants revealed that while there was some evidence of compartmentalization, anatomical barriers do not impose genetic bottlenecks on WNV populations. Together, these data suggest that the complexity of WNV populations are not significantly diminished during the extrinsic incubation period of mosquitoes.
Highlights
West Nile virus (WNV; Flaviviridae, Flavivirus) was introduced into North America in 1999 and has since spread across the continental United States and into Canada, Mexico, the Carribean, and South America [1]
Population bottlenecks during transmission may profoundly influence the evolution of arboviruses by stochastically reducing population variation, thereby selecting random genomes that may be less fit than the overall population
It is unclear whether arboviruses experience genetic bottlenecks during infection of the mosquito vector
Summary
West Nile virus (WNV; Flaviviridae, Flavivirus) was introduced into North America in 1999 and has since spread across the continental United States and into Canada, Mexico, the Carribean, and South America [1]. It was determined that the WN02 genotype requires a shorter extrinsic incubation period in mosquitoes (EIP, time from vector infection to transmission) thereby resulting in an increased vectorial capacity of local mosquitoes. The emergence of Chikungunya virus (CHIKV; Togaviridae, Alphavirus) seems to have been facilitated by analogous mutations that result in increased transmission efficiency by the vector Aedes albopictus [9,10]. Relatively minor consensus genetic changes can significantly influence arbovirus transmission patterns and disease emergence. Determining the mechanistic underpinnings of genetic change in arboviruses is critical to understanding their persistence and emergence
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