Recent studies using molecular genetic approaches have made important contributions to our understanding of the epidemiology of veterinary arboviral encephalitides. Viruses utilizing avian enzootic hosts, such as Western equine encephalitis virus (WEEV) and North American Eastern equine encephalitis virus (EEEV), evolve as relatively few, highly conserved genotypes that extend over wide geographic regions; viruses utilizing mammalian hosts with more limited dispersal evolve within multiple genotypes, each geographically restricted. Similar findings have been reported for Australian alphaviruses. This difference may be related to vertebrate host relationships and the relative mobility of mammals and avians. Whereas EEEV and Venezualan equine encephalitis virus (VEEV) utilize small mammalian hosts in the tropics, most WEEV genotypes probably utilize avian hosts in both North and South America. The ability of mobile, infected avian hosts to disperse alphaviruses may result in continual mixing of virus populations, and thus limit diversification. This high degree of genetic conservation is also exhibited by EEE and Highlands J viruses in North America, where passerine birds serve as amplifying hosts in enzootic transmission foci. Most equine arboviral pathogens, including EEEV, WEEV and Japanese encephalitis virus (JEV), occur in a naturally virulent enzootic state and require only appropriate ecological conditions to cause epizootics and epidemics. However, VEE epizootics apparently require genetic changes to convert avirulent enzootic strains into distinct epizootic serotypes. All of these arboviruses have the potential to cause severe disease of veterinary and human health importance, and further molecular epidemiological studies will undoubtedly improve our ability to understand and control future emergence.
|Original language||English (US)|
|Number of pages||16|
|State||Published - Mar 1999|
ASJC Scopus subject areas
- Animal Science and Zoology