Inhibition of apoptosis prevents West Nile virus cell damage
West Nile Virus (WNV) is a single stranded RNA flavivirus. WNV infection of humans typically results in subclinical or non-specific, mild febrile illnesses. However, about 1 in 150 patients will develop encephalitis and meningitis with high lethality rate due to virus invasion into the central nervous system. Since 1999, the virus has increasingly gained importance in North America as it caused an epizootic among birds and horses and an epidemic of meningitis and encephalitis in humans. To date, no pharmacological treatment options for WNV-infected patients exist. Apoptosis is a highly conserved mode of programmed cell death, commonly mediated by the activation of caspases. Although neurons are regarded as the major target of WNV in vivo, WNV infection has been shown to induce apoptosis in different cell lines in a similar manner in vitro. Recently, it was shown that WNV-infection induces caspase-3 activation and apoptosis in brains of wild-type mice and in primary CNS-derived mouse neurons. WNV infection-induced cell death may contribute to fatal WNV disease. Therefore, thorough knowledge of the molecular mechanism of WNV-induced neural cell death will allow us to better understand the progression of WNV infection and the associated neurological pathology.
We used WNV-infected glioma cells to study WNV-replication and WNV-induced apoptosis in human brain-derived cells. 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.
Inhibition of apoptosis prevents West Nile virus induced cell death
BMC Microbiology 2007 7: 49
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