NDLI: Transcriptional control of HIV latency: Cellular signaling pathways, epigenetics, happenstance and the hope for a cure

Content Provider	PubMed Central
Author	Mbonye, Uri Karn, Jonathan
Copyright Year	2014
Abstract	Replication-competent latent HIV-1 proviruses that persist in the genomes of a very small subset of resting memory T cells in infected individuals under life-long antiretroviral therapy present a major barrier towards viral eradication. Multiple molecular mechanisms are required to repress the viral trans-activating factor Tat and disrupt the regulatory Tat feedback circuit leading to the establishment of the latent viral reservoir. In particular, latency is due to a combination of transcriptional silencing of proviruses via host epigenetic mechanisms and restrictions on the expression of P-TEFb, an essential co-factor for Tat. Induction of latent proviruses in the presence of antiretroviral therapy is expected to enable clearance of latently infected cells by viral cytopathic effects and host antiviral immune responses. An in-depth comprehensive understanding of the molecular control of HIV-1 transcription should inform the development of optimal combinatorial reactivation strategies that are intended to purge the latent viral reservoir.
Related Links	http://dx.doi.org/10.1016/j.virol.2014.02.008
Ending Page	339
Page Count	12
Starting Page	328
File Format	PDF
ISSN	10960341
e-ISSN	10960341
Journal	Virology
Volume Number	0
Language	English
Publisher Date	2014-04-01
Access Restriction	Open
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Virology

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Transcriptional control of HIV latency: Cellular signaling pathways, epigenetics, happenstance and the hope for a cure