Journal
CELL HOST & MICROBE
Volume 17, Issue 6, Pages 736-740Publisher
CELL PRESS
DOI: 10.1016/j.chom.2015.05.010
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Funding
- National Institutes of Health [R21 AI110263, R21 AI114335, R21 AI116173, R56 AI108467, Baylor-UTHouston CFAR: P30 AI036211]
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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.
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