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Sindbis virus induces apoptosis through a caspase-dependent, CrmA-sensitive pathway
V E Nava1, A Rosen, M A Veliuona
1Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Public Health, Baltimore, Maryland 21205, USA.
Journal of Virology
|January 7, 1998
Summary
Sindbis virus triggers apoptosis, a form of programmed cell death, by activating caspases. Inhibiting these caspases with CrmA or zVAD-FMK protected infected cells and improved survival rates in mice.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Sindbis virus infection induces apoptosis in cultured cells and mouse neurons.
- The precise mechanism of Sindbis virus-mediated apoptosis activation remains unclear.
Purpose of the Study:
- To investigate the role of caspases in Sindbis virus-induced apoptosis.
- To determine if caspase inhibition can protect against Sindbis virus-induced cell death and improve survival.
Main Methods:
- Utilized specific caspase inhibitors, CrmA and zVAD-FMK, to study Sindbis virus-induced cell death.
- Assessed the impact of inhibitors on cell survival in infected cultures and mice.
- Analyzed whether inhibitors affected viral replication or viral proteases.
Main Results:
- Caspase inhibitors CrmA and zVAD-FMK significantly reduced Sindbis virus-induced cell death.
- CrmA treatment markedly increased the survival rate of infected mice.
- Inhibitor efficacy suggests they target the cellular apoptotic pathway, not viral replication or proteases.
Conclusions:
- Cellular caspases play a critical role in mediating Sindbis virus-induced apoptosis.
- The Sindbis virus apoptotic pathway shares similarities with Fas or TNF-alpha-induced death pathways.
- Targeting caspases represents a potential therapeutic strategy against Sindbis virus infection.