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Diverse apoptotic pathways in enterovirus 71-infected cells
Shih-Cheng Chang1, Jing-Yi Lin, Lily Yen-cheng Lo
1Graduate Institute of Basic Medical Sciences, Chang Gung University, Tao-Yuan, Taiwan.
Journal of Neurovirology
|March 16, 2005
Summary
Enterovirus 71 infection triggers apoptosis in neural and non-neural cells. The mitochondrial pathway, involving caspase 9, is key, particularly in neural cells during enterovirus 71 neuropathogenesis.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- The neuropathogenesis of enterovirus 71 (EV71) infection is not fully understood.
- Investigating apoptotic pathways is crucial for understanding EV71's impact on neural and non-neural cells.
Purpose of the Study:
- To comprehensively study the apoptotic pathways activated by enterovirus 71 infection in both neural and non-neural cell lines.
- To elucidate the specific mechanisms of cell death induced by EV71.
Main Methods:
- Infection of human glioblastoma (SF268), human neuroblastoma (SK-N-MC), RD, and Vero cells with enterovirus 71.
- Assessment of classical cytopathic effects and apoptosis markers (DNA fragmentation, phosphatidylserine translocation).
- Analysis of mitochondrial pathway activation (cytochrome c efflux, caspase 9 cleavage) and extrinsic pathway markers (caspase 8 activation, Bid cleavage).
Main Results:
- Enterovirus 71 induced cytopathic effects and apoptosis in all tested cell lines.
- Mitochondrial apoptosis pathway activation (cytochrome c efflux, caspase 9 cleavage) was observed in all infected cells.
- The extrinsic apoptosis pathway (caspase 8 activation, Bid cleavage) was specifically activated in non-neural cells.
Conclusions:
- A mitochondrial apoptosis pathway, mediated by caspase 9, is a primary mechanism in enterovirus 71-induced cell death.
- This pathway is particularly significant in enterovirus 71-infected neural cells, contributing to neuropathogenesis.