Japanese encephalitis (JE) virus causes an encephalitic disease in humans that is characterized by a wide range of symptoms from a nonspecific febrile illness to convulsions, seizure, and death (Solomon et al. 2000). Approximately 30% of patients presenting at hospital with JE will succumb to the disease and about 50% of those who survive will have severe neurological sequelae (Solomon et al. 2000). The JE virus is carried by mosquitoes, primarily Culex species, and is endemic from tropical to temperate regions of Asia and Australasia. JE virus is generally considered to circulate in an endemic cycle in southern regions of Asia whereas the virus tends to have a more epidemic epidemiological pattern in northern Asia with outbreaks occurring during the summer months (Vaughn and Hoke 1992). The virus infects a number of animal hosts, most importantly pigs, which act as amplifying hosts and are found in high numbers throughout rural Asia. The first isolate of JE virus, and the prototype strain, was isolated in 1935 in Tokyo from a human brain and is designated the Nakayama strain. Since that time, a large number of JE virus isolates have been identified from a wide range of geographical locales throughout Asia, Indonesia, and most recently, northern Australia. Many of these viruses have been analyzed serologically and/or genetically to examine the distribution of the virus strains over both temporal and geographical boundaries. To date, the complete genome of 20 strains of JE virus have been sequenced including the first isolate from Australia (Williams et al. 2000).