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- W2562209318 abstract "Japanese encephalitis virus (JEV), a typical cytoplasmic RNA virus, has been utilized by us for intensive study of virus-cell interaction. Infection of JEV often causes severe cytopathic effects and cell death from its targets, at least in part, if not all, due to occurrence of apoptosis. Enforced expression of human bcl-2, although does not inhibit virus production, delays JEV-induced apoptotic process in infected fibroblast BHK-21 but not neuronal N18 cells, and as result, some infected BHK-21 cells are survival and become persistently infected even after a long-term culture. JEV infection can quickly induce the target cells to activate NF-κB pathway, which, on the other hand, appears not to be required for JEV replication. In addition, JEV triggers the unfolded protein response (UPR), thereby inducing CHOP/GADD153 expression and p38 MAP kinase activation. Interestingly, bcl-2 overexpression and treatment by a pan-caspase inhibitor, z-VAD-fmk, inhibited CHOP induction and consequently diminished JEV-induced apoptosis, suggesting that Bcl-2 and caspases could be the upstream regulator of CHOP. These observations suggest that virus-induced UPR may participate, via p38-dependent and CHOP-mediated pathways, in the apoptotic process triggered by JEV infection." @default.
- W2562209318 created "2017-01-06" @default.
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- W2562209318 date "2002-08-01" @default.
- W2562209318 modified "2023-09-23" @default.
- W2562209318 title "Interactions between Japanese Encephalitis Virus and its Target Cells" @default.
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