Regulation of HIV-1 latency by chromatin structure and nuclear architecture

Current antiretroviral therapies fail to cure HIV-1 (human immunodeficiency virus type 1) infection because HIV-1 persists as a transcriptionally inactive provirus in resting memory CD4+ T cells. Multiple molecular events are known to regulate HIV-1 gene expression, yet the mechanisms governing the...

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Bibliographic Details
Main Authors: Lusic, Marina (Author) , Giacca, Mauro (Author)
Format: Article (Journal)
Language:English
Published: 13 February 2015
In: Journal of molecular biology
Year: 2015, Volume: 427, Issue: 3, Pages: 688-694
ISSN:1089-8638
DOI:10.1016/j.jmb.2014.07.022
Online Access:Verlag, Volltext: http://dx.doi.org/10.1016/j.jmb.2014.07.022
Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S0022283614003702
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Author Notes:Marina Lusic and Mauro Giacca
Description
Summary:Current antiretroviral therapies fail to cure HIV-1 (human immunodeficiency virus type 1) infection because HIV-1 persists as a transcriptionally inactive provirus in resting memory CD4+ T cells. Multiple molecular events are known to regulate HIV-1 gene expression, yet the mechanisms governing the establishment and maintenance of latency remain incompletely understood. Here we summarize different molecular aspects of viral latency, from its establishment in resting CD4+ T cells to the mechanisms involved in the reactivation of latent viral reservoirs. We focus on the relevance of chromatin structure and nuclear architecture in determining the transcriptional fate of integrated HIV-1 genomes, in light of recent findings indicating that proximity to specific subnuclear neighborhoods regulates HIV-1 gene expression.
Item Description:Gesehen am 17.07.2017
Physical Description:Online Resource
ISSN:1089-8638
DOI:10.1016/j.jmb.2014.07.022