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Vaccinia Virus Arrests and Shifts the Cell Cycle
Caroline K Martin1, Jerzy Samolej2, Annabel T Olson3
1MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK.
Viruses
|February 26, 2022
Summary
Vaccinia virus (VACV) infection inhibits cell proliferation and alters the host cell cycle. Viral early genes cause inhibition, while later genes shift the cell cycle, involving specific viral kinases and effector proteins.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Viruses commonly manipulate the host cell cycle for replication.
- Vaccinia virus (VACV) is known to alter cell cycle regulation and trigger DNA damage responses.
Purpose of the Study:
- Investigate VACV's effect on host cell proliferation and cell cycle progression.
- Identify viral factors responsible for cell cycle dysregulation.
Main Methods:
- Utilized VACV mutants to determine infection stages and viral effectors.
- Analyzed cell proliferation and cell cycle progression.
- Assessed DNA damage checkpoint activation and effector degradation.
Main Results:
- VACV inhibits cell proliferation and shifts the host cell cycle independently.
- Viral early genes inhibit proliferation; post-replicative genes shift the cell cycle.
- Viral kinase F10 activates the DNA damage checkpoint; B1/B12 mediate p53/p21 degradation.
Conclusions:
- VACV employs temporal expression of multiple effector proteins to modulate host cell proliferation and cell cycle.
- Viral kinases F10, B1, and B12 are key players in VACV-induced cell cycle manipulation.
- Understanding these mechanisms provides insight into viral strategies for host manipulation.
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