Abstract
To establish a productive infection, HIV-1 must counteract cellular innate immune mechanisms and redirect cellular processes toward viral replication. Recent studies have discovered that HIV-1 and other primate immunodeficiency viruses subvert cell cycle regulatory mechanisms to achieve these ends. The viral Vpr and Vpx proteins target cell cycle controls to counter innate immunity. The cell-cycle-related protein Cyclin L2 is also utilized to counter innate immunity. The viral Tat protein utilizes Cyclin T1 to activate proviral transcription, and regulation of Cyclin T1 levels in CD4(+) T cells has important consequences for viral replication and latency. This review will summarize this emerging evidence that primate immunodeficiency viruses subvert cell cycle regulatory mechanisms to enhance replication.
Copyright © 2015 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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CD4-Positive T-Lymphocytes / virology
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Cell Cycle / physiology*
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Cyclin T / metabolism
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Cyclins / metabolism
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HIV-1 / pathogenicity*
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HIV-1 / physiology
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Host-Pathogen Interactions*
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Humans
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Immunity, Innate
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Monomeric GTP-Binding Proteins / metabolism
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Recombinases / metabolism
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SAM Domain and HD Domain-Containing Protein 1
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Transcription Factors / metabolism
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Viral Regulatory and Accessory Proteins / metabolism
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tat Gene Products, Human Immunodeficiency Virus / metabolism
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vpr Gene Products, Human Immunodeficiency Virus / metabolism
Substances
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CCNL2 protein, human
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Cyclin T
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Cyclins
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Recombinases
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Transcription Factors
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VPX protein, Human immunodeficiency virus 2
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Viral Regulatory and Accessory Proteins
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tat Gene Products, Human Immunodeficiency Virus
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vpr Gene Products, Human Immunodeficiency Virus
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vpr protein, Human immunodeficiency virus 1
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SLX4 protein, human
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SAM Domain and HD Domain-Containing Protein 1
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SAMHD1 protein, human
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Monomeric GTP-Binding Proteins