Cellular Players in the Herpes Simplex Virus Dependent Apoptosis Balancing Act
Author Information
Author(s): Nguyen Marie L., Blaho John A.
Primary Institution: Des Moines University, Des Moines, IA, USA; Mount Sinai School of Medicine, New York, NY, USA
Hypothesis
The study investigates how cellular genes regulate sensitivity to herpes simplex virus (HSV)-dependent apoptosis.
Conclusion
The study reveals that apoptosis is initially triggered during HSV infection but is later blocked by viral anti-apoptotic factors, creating a balance that affects viral replication.
Supporting Evidence
- HSV infection triggers apoptosis early but later produces anti-apoptotic proteins to block cell death.
- Cell-type differences in response to HSV-induced apoptosis indicate the importance of cellular factors.
- Specific cellular genes, including caspases and Bcl-2 family members, modulate the apoptotic response during HSV infection.
Takeaway
When the herpes virus infects cells, it can make them die or stay alive depending on how it tricks the cell's death signals.
Methodology
The review summarizes existing research on the role of cellular genes in regulating apoptosis during HSV infection.
Limitations
The review primarily focuses on existing studies and may not cover all aspects of HSV-induced apoptosis.
Digital Object Identifier (DOI)
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