This review discusses the global dynamics of West Nile virus (WNV) infection. Originally considered a childhood illness, WNV infection has recently emerged as a cause of severe neurologic disease. WNV was originally isolated from Uganda and has been described on almost every continent. There are 5 lineages, and lineage type does not correlate with geographic distribution; all major human encephalitis outbreaks have occurred secondary to lineage 1. Transmission occurs between Culex species mosquitos and a passeriform avian host; mammals such as humans and horses are usually “dead end” hosts. Human clinical disease ranges from asymptomatic infection to West Nile fever (fever, chills, rash, headache, myalgia, nausea) to severe neurologic disease. The latter is frequently seen in elderly individuals and was identified in 1994.
Bird mortality is a novel finding in the epidemiology of infection in North America and Israel. WNV has also been isolated from a variety of mosquito species in the New World. Avian virulence mutations associated with major disease outbreaks have been identified, and such virulence may result in increased transmission due to high viremia and the potential to replicate at a variety of temperatures. Such mutations are probably the result of adaptive pressure toward increased viral replication and transmission. These characteristics suggest rapid adaptation to different vertebrate hosts, invertebrate arthropod vectors, temperatures, and conditions to allow for sustained transmission and propagation.
COMMENTARY: WNV infection has received significant recent attention because of clinical courses with high morbidity in the United States. This review illustrates the fluid adaptive nature of the virus and its diverse virulence characteristics, hosts, and vectors. It also underscores the importance of appropriate mosquito control for mammalian hosts, including dogs, horses, and humans.
Changing patterns of West Nile virus transmission: Altered vector competence and host susceptibility. Brault AC. VET RES 40:43, 2009.