Abstract

The first clinical isolate of the Japanese encephalitis virus was prepared in 1933 from human brain tissue in rabbits and was initially referred to as Japanese “B” encephalitis virus to indicate its association with the “B” or summer type of epidemic encephalitis in Japan. Neurovirulence of the JE virus (JEV) involves a combination of infection and dysfunction of neurons, caused by direct viral damage, and indirect damage mediated by the generation of an inflammatory milieu in the Central nervous system, and other mechanisms such as apoptosis. Human infections of Japanese encephalitis are common throughout the endemic region. Infection with JEV may be asymptomatic or manifest as a mild febrile illness, aseptic meningitis, or classic severe meningomyeloencephalitis. A young adult man, who received four doses of JEV (Nakayama strain) vaccination in childhood, reportedly developed acute JEV infection that was characterized with acute flaccid paralysis.

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