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Use of In vivo Imaging to Monitor the Progression of Experimental Mouse Cytomegalovirus Infection in Neonates
Published on: July 6, 2013
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Human cytomegalovirus riding the cell cycle
1Department of Cellular and Molecular Medicine, The Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, La Jolla, CA, 92093-0712, USA, dspector@ucsd.edu.
Medical Microbiology and Immunology
|March 18, 2015
Summary
Human cytomegalovirus (HCMV) manipulates the host cell cycle, driving cells to G1 phase for viral replication. HCMV infection alters cell cycle proteins and pathways to favor viral DNA synthesis over host DNA replication.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Human cytomegalovirus (HCMV) primarily infects quiescent cells, necessitating cell cycle modulation for replication.
- HCMV infection redirects host cell machinery to support viral gene expression, DNA replication, and virion production.
Purpose of the Study:
- To review the intricate effects of HCMV infection on host cell cycle regulatory pathways.
- To highlight key viral proteins responsible for manipulating the host cell cycle.
Main Methods:
- Analysis of molecular mechanisms including altered RNA transcription and protein modifications.
- Investigation of changes in cyclin-dependent kinases and ubiquitin-proteasome pathway activity.
- Examination of protein localization and signaling pathway alterations during infection.
Main Results:
- HCMV infection forces cells into G0/G1 phase, optimizing conditions for viral DNA synthesis.
- Viral strategies subvert host cell functions, prioritizing viral DNA replication.
- HCMV targets the anaphase-promoting complex to degrade key cell cycle proteins, preventing host DNA synthesis.
Conclusions:
- HCMV infection profoundly alters host cell cycle progression to create a favorable replication environment.
- Viral proteins play a critical role in hijacking cell cycle control, ensuring efficient viral replication.
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