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Herpes simplex virus UL14 protein blocks apoptosis.
Yohei Yamauchi1, Tohru Daikoku, Fumi Goshima
1Laboratory of Virology, Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Aichi 466-8550, Japan.
Microbiology and Immunology
|October 31, 2003
Summary
The herpes simplex virus type 2 UL14 protein enhances cell resistance to apoptosis. This protein
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Apoptosis, or programmed cell death, is a critical cellular process.
- Herpes simplex virus (HSV) encodes proteins that can modulate host cell apoptosis.
- The specific role of HSV-2 UL14 protein in apoptosis regulation is not fully understood.
Purpose of the Study:
- To investigate the anti-apoptotic function of the HSV-2 UL14 protein.
- To compare the effects of HSV-1 and HSV-2 UL14 proteins on apoptosis.
Main Methods:
- Generation of a cell line stably expressing HSV-2 UL14 protein (14/HEp-2).
- Induction of apoptosis using osmotic shock and specific drugs.
- Analysis of apoptosis in parental and UL14-expressing cells.
- Comparison of apoptosis inhibition by HSV-1 UL14 deletion virus (UL14D) and rescued virus (UL14R).
Main Results:
- The 14/HEp-2 cell line exhibited increased resistance to drug- and osmotic shock-induced apoptosis compared to the parental cell line.
- HSV-1 UL14D demonstrated significantly weaker inhibition of apoptosis than the UL14R virus.
- These findings suggest a conserved anti-apoptotic role for the UL14 protein across HSV types.
Conclusions:
- The HSV-2 UL14 protein possesses significant anti-apoptotic properties.
- The UL14 protein's function may be linked to its structural or functional similarities with heat shock proteins.
- Further research into UL14 protein's mechanism could reveal novel therapeutic targets for viral infections and cancer.