West Nile Virus Infection in the Golden Hamster

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´╗┐West Nile Virus Infection in the Golden Hamster
This report describes a new hamster model for West Nile (WN) virus encephalitis. Following intraperitoneal inoculation of a New York isolate of WN virus, hamsters had moderate viremia of 5 to 6 days in duration, followed by the development of humoral antibodies. Encephalitic symptoms began 6 days after infection; about half the animals died between the seventh and 14th days. The appearance of viral antigen in the brain and neuronal degeneration also began on the sixth day. WN virus was cultured from the brains of convalescent hamsters up to 53 days after initial infection, suggesting that persistent virus infection occurs. Hamsters offer an inexpensive model for studying the pathogenesis and treatment of WN virus encephalitis.

West Nile (WN) virus was first detected in North America in the summer of 1999, during an epidemic and epizootic involving humans, horses, and birds in the New York City metropolitan area. The persistence and spread of the virus to several neighboring states during the summer and fall of 2000 suggest that WN virus is now endemic in the United States and that its geographic range probably will continue to expand. Although many WN virus infections in humans are asymptomatic or unrecognized, some patients have an acute denguelike illness, and a small percentage have frank meningitis and encephalitis. The latter complication is most common among the elderly, with recent case-fatality rates ranging from 4% to 11%.

WN virus is a positive-stranded RNA virus; based on its antigenic and genetic characteristics, it is included in the Japanese encephalitis (JE) serocomplex of the genus Flavivirus, family Flaviviridae. WN virus was originally isolated from a febrile patient in Uganda in 1937, but it has a worldwide geographic distribution, including most of Africa, southern Europe, central and southern Asia, Oceania, and now North America. Despite its wide geographic distribution and frequency, little is known about the pathogenesis of human infection with WN virus, especially encephalitis. One unique pathologic finding in WN virus encephalitis, unlike the encephalitides caused by other closely related flaviviruses, is the targeting of Purkinje cells of the cerebellum. We describe preliminary studies of a hamster model for the disease.

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