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Medical Microbiology and Immunology : Volume 204, Issue 2, April 2015

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Human cytomegalovirus riding the cell cycle

Content Provider	Springer Nature Link
Author	Spector, Deborah H.
Copyright Year	2015
Abstract	Human cytomegalovirus (HCMV) infection modulates the host cell cycle to create an environment that is optimal for viral gene expression, DNA replication, and production of infectious virus. The virus mostly infects quiescent cells and thus must push the cell into G1 phase of the cell cycle to co-opt the cellular mechanisms that could be used for DNA synthesis. However, at the same time, cellular functions must be subverted such that synthesis of viral DNA is favored over that of the host. The molecular mechanisms by which this is accomplished include altered RNA transcription, changes in the levels and activity of cyclin-dependent kinases, and other proteins involved in cell cycle control, posttranslational modifications of proteins, modulation of protein stability through targeted effects on the ubiquitin–proteasome degradation pathway, and movement of proteins to different cellular locations. When the cell is in the optimal G0/G1 phase, multiple signaling pathways are altered to allow rapid induction of viral gene expression once negative factors have been eliminated. For the most part, the cell cycle will stop prior to initiation of host cell DNA synthesis (S phase), although many cell cycle proteins characteristic of the S/G2/M phase accumulate. The environment of a cell progressing through the cell cycle and dividing is not favorable for viral replication, and HCMV has evolved ways to sense whether cells are in S/G2 phase, and if so, to prevent initiation of viral gene expression until the cells cycle back to G1. A major target of HCMV is the anaphase-promoting complex E3 ubiquitin ligase, which is responsible for the ubiquitination and subsequent degradation of cyclins A and B and other cell cycle proteins at specific phases in the cell cycle. This review will discuss the effects of HCMV infection on cell cycle regulatory pathways, with the focus on selected viral proteins that are responsible for these effects.
Starting Page	409
Ending Page	419
Page Count	11
File Format	PDF
ISSN	03008584
Journal	Medical Microbiology and Immunology
Volume Number	204
Issue Number	3
e-ISSN	14321831
Language	English
Publisher	Springer Berlin Heidelberg
Publisher Date	2015-03-17
Publisher Place	Berlin/Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Human cytomegalovirus Cell cycle Anaphase-promoting complex Cyclins Cyclin-dependent kinases Medical Microbiology Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Microbiology (medical)

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