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BMC Microbiol. 2007 May 29;7:49.

Inhibition of apoptosis prevents West Nile virus induced cell death.

Author information

  • 1Institute for Medical Virology, Johann Wolfgang Goethe-University, Frankfurt am Main, Germany. malte-kleinschmidt@gmx.de <malte-kleinschmidt@gmx.de>

Abstract

BACKGROUND:

West Nile virus (WNV) infection can cause severe meningitis and encephalitis in humans. Apoptosis was recently shown to contribute to the pathogenesis of WNV encephalitis. Here, we used WNV-infected glioma cells to study WNV-replication and WNV-induced apoptosis in human brain-derived cells.

RESULTS:

T98G cells are highly permissive for lytic WNV-infection as demonstrated by the production of infectious virus titre and the development of a characteristic cytopathic effect. WNV replication decreased cell viability and induced apoptosis as indicated by the activation of the effector caspase-3, the initiator caspases-8 and -9, poly(ADP-ribose)polymerase (PARP) cleavage and the release of cytochrome c from the mitochondria. Truncation of BID indicated cross-talk between the extrinsic and intrinsic apoptotic pathways. Inhibition of the caspases-8 or -9 inhibited PARP cleavage, demonstrating that both caspases are involved in WNV-induced apoptosis. Pan-caspase inhibition prevented WNV-induced apoptosis without affecting virus replication.

CONCLUSION:

We found that WNV infection induces cell death in the brain-derived tumour cell line T98G by apoptosis under involvement of constituents of the extrinsic as well as the intrinsic apoptotic pathways. Our results illuminate the molecular mechanism of WNV-induced neural cell death.

PMID:
17535425
[PubMed - indexed for MEDLINE]
PMCID:
PMC1891299
Free PMC Article
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