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Herpes simplex virus infection and apoptosis.
Margot L Goodkin1, Elise R Morton, John A Blaho
1Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA.
International Reviews of Immunology
|December 24, 2003
Summary
Human herpes simplex virus (HSV) infection triggers apoptosis, a programmed cell death, but also produces proteins to prevent it. This review details how HSV manipulates cell death during infection.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Human herpes simplex virus (HSV) infection has significant cellular consequences.
- HSV infection can induce apoptosis, a critical cellular process.
- Cells infected by HSV synthesize proteins to counteract apoptosis.
Purpose of the Study:
- To review recent findings on HSV's modulation of apoptosis.
- To clarify the mechanisms by which HSV induces and prevents apoptosis.
- To highlight the multicomponent nature of HSV's control over programmed cell death.
Main Methods:
- Review of recent scientific literature and data.
- Analysis of molecular mechanisms involved in apoptosis.
- Examination of viral protein functions in cellular processes.
Main Results:
- HSV infection actively induces apoptosis in host cells.
- HSV synthesizes specific proteins to inhibit the apoptotic process.
- The modulation of apoptosis by HSV is a complex, multifaceted phenomenon.
Conclusions:
- HSV employs a sophisticated strategy to control host cell death.
- Understanding HSV's manipulation of apoptosis is key to comprehending viral pathogenesis.
- Further research into these mechanisms can inform therapeutic strategies against HSV.