INTRODUCTIONThe adaptive potential of RNA viruses is driven by error-prone replication which creates a heterogeneous swarm of virus genotypes within each host (1). RNA arthropod-borne viruses (arboviruses) therefore have the potential for rapid evolution but exhibit high degrees of consensus genome sequence stability in nature [summarized in reference (2)]. The need to navigate distinct host environments and barriers to infection and transmission is believed to restrict arbovirus evolution. Indeed, the fitness trade-off hypothesis for arboviruses posits that fitness gains in one host come at the cost of fitness losses in the other host. Paradoxically, a preponderance of experimental evidence suggests that host alternation does not automatically limit the adaptive potential of arboviruses [reviewed in references (3) and (4)]. Rather, arboviruses may be the ultimate generalists, evolving mechanisms to limit or avoid the effects of trade-offs from dual-host cycling. They may be positioned to evolve rapidly when novel conditions arise.This is perhaps best exemplified by the fact that many arbovirus epidemics have been associated with virus genetic change. For example, Indian Ocean lineage chikungunya virus adaptation to Aedes albopictus was mediated by a series of envelope glycoprotein E2/E3 and E1 substitutions during an explosive outbreak on La Reunion Island (5, 6). Other examples of epidemic-enhancing mutations include West Nile virus adaptation for more efficient transmission by North American mosquitoes (7) and Venezuelan equine encephalitis virus adaptations that produce high viral titers in horses (8). Finally, considerable research effort has been dedicated to identifying mutations that may have contributed to Zika
Gain without pain: adaptation and increased virulence of Zika virus in vertebrate host without fitness cost in mosquito vector
