©2006 RKD Peterson

Initially isolated in 1937 in Uganda (Smithburn et al. 1940), West Nile virus (WNV) is a single-stranded RNA virus of the family Flaviridae (Campbell et al. 2002, Petersen and Marfin 2002), which belongs to the Japanese encephalitis serocomplex, and includes other viruses such as Japanese encephalitis, Murray Valley encephalitis, and St. Louis encephalitis viruses (Petersen and Marfin 2002, Depoortere et al. 2004). There are two lineages of West Nile strains (Jia et al. 1999, Lanciotti et al. 1999, Scherret et al. 2001): viruses from lineage 1 were associated with the main recent human encephalitis epidemics and have been isolated from Africa, India, Europe, and North America (Petersen and Roehrig 2001, McLean et al. 2002); viruses from lineage 2 have been identified only in sub-Saharan Africa and Madagascar (Lanciotti et al. 2002, McLean et al. 2002). The WNV strain responsible for the outbreak in the United States in 1999 was identified as a lineage 1 virus that circulated in Israel from 1997 to 2000 (Lanciotti et al. 1999, Giladi et al. 2001), and phylogenetic analysis of complete genomes confirmed the close relationship between American strains and certain Israeli strains (Charrel et al. 2003), which suggests that the virus was imported into North America from the Middle East (Jia et al. 1999, Petersen and Roehrig 2001). Very few genetic changes were observed in the variant of WNV circulating in the United States since its introduction in 1999 (Petersen and Marfin 2002). However, disease severity and frequency appears to have been changing since the mid-1990s (Petersen and Roehrig 2001), although it is not clear whether the observed changes are due to differences in the circulating virus's virulence or to changes in age structure, background immunity, or predisposing conditions in the affected populations (Hubalek 2001, Petersen and Roehrig 2001).

WNV is maintained in an enzootic transmission cycle where wild and domestic birds are the main amplifying hosts and ornithophilic mosquitoes are the main vectors. Since its introduction into North America in 1999, WNV has been detected in at least 43 mosquito species (CDC 2003). However, not all of those are competent vectors of WNV (Turell et al. 2005). Species in the Culex pipiens complex may serve as bridge vectors of WNV from birds to humans (Spielman 2001). Kilpatrick et al. (2005) suggest that the most important mosquito species for transmission of WNV to humans in the northeastern and north-central United States are Cx. pipiens and Cx. restuans. These species breed primarily in tires, gutters, catch basins, and polluted surface pools (Pratt and Moore 1993), where mosquito control efforts should then be focused, reducing the detrimental effects on nontarget species, and improving the effectiveness of control measures (Kilpatrick et al. 2005). In the southeastern United States, the major vectors of WNV among birds are Cx. quinquefasciatus and Cx. nigripalpus (Sardelis et al. 2001, Rutledge et al. 2003), while Cx. tarsalis and Cx. quinquefasciatus are primary vectors among birds in the western United States (Goddard et al. 2002). Species in the Cx. pipiens complex can transmit the virus transovarially (Dohm et al. 2002), so overwintering mosquitoes can initiate another infection cycle the next spring (Nasci et al. 2001).

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