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Published online ahead of print on 4 March 2009 as doi:10.1099/vir.0.008045-0
Journal of General Virology 2009;90:818.

A more recent version of this article appeared on April 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.008045-0
© 2009 Society for General Microbiology
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Japanese encephalitis virus produces a CD4-Th2 response and associated immunoprotection in an adoptive transfer murine model

S. Moanaro Biswas, Vijay M Ayachit, Gajanan N Sapkal, Shubhangi A Mahamuni and Milind M Gore1

National Institute of Virology

1 E-mail: milind_gore{at}hotmail.com

Japanese encephalitis (JE) is an acute infection of the central nervous system (CNS) caused by the Japanese encephalitis virus (JEV). The importance of an effective humoral response in preventing JEV infection has already been established, while the contribution of cellular immunity remains unclear. In this study, we have used an experimental murine model to understand the protective effects of cell-mediated immunity in JEV infection. 14-day-old mice adoptively transferred with JEV immune splenocytes were seen to be protected from peripheral JEV challenge. The survival rate was reduced when transferred cells were depleted of the CD4+ T cell population. Correspondingly, increased protection was observed when JEV primed CD4+ isolated T cells were transferred as compared to CD8+ isolated T cells. Mice protected from JEV infection by the adoptive transfer of JEV immune splenocytes had higher levels of immunomodulatory cytokines and decreased expression of proinflammatory cytokines. Concurrent with the increase in Th2 cytokines, JEV specific IgM and IgG1 antibody titers were seen to be elevated in protected mice. Taken together, these data indicated a definite role for CD4+ T cells in protection from lethal JEV infection in naïve 14-day-old mice. Induction of a Th2 cytokine response and IgG1 antibody probably achieved an immunomodulatory effect that resulted in the enhanced survival of these animals.

Received 19 October 2008; accepted 18 December 2008.




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