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West Nile virus-induced bax-dependent apoptosis
M C Parquet1, A Kumatori, F Hasebe
1Department of Virology, Institute of Tropical Medicine, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
FEBS Letters
|July 4, 2001
Summary
West Nile virus (WNV) infection triggers apoptosis, a form of programmed cell death, in human cells. Viral replication is necessary for WNV to induce these cell-death pathways.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- West Nile virus (WNV) causes febrile illness and encephalitis in humans.
- Understanding WNV-induced cell death mechanisms is crucial for therapeutic development.
Purpose of the Study:
- To investigate the mechanism of cell death induced by West Nile virus (WNV).
- To determine if viral replication is required for WNV-induced apoptosis.
Main Methods:
- WNV infection of K562 and Neuro-2a cell lines.
- Flow cytometry to detect apoptosis hallmarks (cell shrinkage, chromatin condensation, subdiploid DNA).
- Analysis of DNA fragmentation and cell membrane phospholipid changes.
- Use of UV-inactivated WNV to assess the role of viral replication.
Main Results:
- WNV infection induced typical apoptotic features in K562 and Neuro-2a cells.
- DNA fragmentation and altered cell membrane phospholipids were observed in infected K562 cells.
- UV-inactivated WNV did not induce apoptosis, indicating viral replication is essential.
- WNV-induced apoptosis correlated with increased bax gene expression.
Conclusions:
- West Nile virus (WNV) actively induces apoptosis in infected cells.
- Viral replication is a prerequisite for WNV-mediated apoptosis.
- The bax gene is involved in the apoptotic signaling pathway activated by WNV.
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