Abstract

Japanese encephalitis (JE) is a severe and acute encephalitis with a high fatality rate, caused by Japanese encephalitis virus (JEV), a mosquito-borne flavivirus of the genus Flavivirus, family Flaviviridae. The JEV serogroup of flaviviruses includes West Nile virus, St. Louis encephalitis virus, and Murray Valley encephalitis virus which also cause encephalitis, though with some clinical variation (Mackenzie et al., 2007). JE is a major public health problem in the Asian region, accounting for more than 16,000 reported cases and 5,000 deaths annually. With the near eradication of poliomyelitis, JE is now the leading cause of childhood viral neurological infection and disability in Asia (Halstead and Jacobson, 2003). Approximately half of all survivors suffer from permanent neurological and/or mental impairments due to the invasion and destruction of cortical neurons and Purkinje cells by the virus (Johnson et al., 1985, Monath, 1986). Historically, severe epidemics of JE had been reported during the summer season in Japan since the 19th Century and more than 1000 cases were reported annually in the 1960s. With the control of epidemics in Japan and Korea due to changes in agricultural and animal husbandry practices, and in part through vaccination, the number of JE cases markedly

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