Abstract
Transcription of the integrated HIV provirus is subject to regulation by chromatin organization and must employ host cell transcription factors and chromatin modifying complexes to promote the formation of latency, and then reverse this process to replicate in response to T cell activation. The repressed latent HIV-1 proviral 5 LTR is organized into a defined structure where two de-acetylated and positioned nucleosomes flank the enhancer region, presumably imposing a block to transcriptional initiation and elongation. LTR-associated nucleosomes undergo further histone H3 K9 trimethylation, to cause silencing by recruitment of HP1. In this article, we review current understanding of how the transcriptionally silenced provirus might be established through the function of transcription factors that bind conserved ciselements, including SP1, YY1, NF-κB, CBF-1 and RBF-2 (USF/TFII-I), and propose mechanisms by which factors bound to the repressed LTR can enable reactivation in response to cell signaling.
Keywords: HIV-1, chromatin structure, nucleosome positioning, transcription factors, histone modification, cell signaling
Current HIV Research
Title: Factors Controlling Chromatin Organization and Nucleosome Positioning for Establishment and Maintenance of HIV Latency
Volume: 6 Issue: 4
Author(s): Ivan Sadowski, Pedro Lourenco and Tom Malcolm
Affiliation:
Keywords: HIV-1, chromatin structure, nucleosome positioning, transcription factors, histone modification, cell signaling
Abstract: Transcription of the integrated HIV provirus is subject to regulation by chromatin organization and must employ host cell transcription factors and chromatin modifying complexes to promote the formation of latency, and then reverse this process to replicate in response to T cell activation. The repressed latent HIV-1 proviral 5 LTR is organized into a defined structure where two de-acetylated and positioned nucleosomes flank the enhancer region, presumably imposing a block to transcriptional initiation and elongation. LTR-associated nucleosomes undergo further histone H3 K9 trimethylation, to cause silencing by recruitment of HP1. In this article, we review current understanding of how the transcriptionally silenced provirus might be established through the function of transcription factors that bind conserved ciselements, including SP1, YY1, NF-κB, CBF-1 and RBF-2 (USF/TFII-I), and propose mechanisms by which factors bound to the repressed LTR can enable reactivation in response to cell signaling.
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Cite this article as:
Sadowski Ivan, Lourenco Pedro and Malcolm Tom, Factors Controlling Chromatin Organization and Nucleosome Positioning for Establishment and Maintenance of HIV Latency, Current HIV Research 2008; 6 (4) . https://dx.doi.org/10.2174/157016208785132563
DOI https://dx.doi.org/10.2174/157016208785132563 |
Print ISSN 1570-162X |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4251 |
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