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Abstract
Current antiretroviral therapy for HIV‐1 infection effectively suppresses but does not eradicate HIV‐1. Patients on Highly Active Anti‐Retroviral Therapy (HAART) maintain a persistent low‐level viremia requiring lifelong adherence to antiretroviral therapies. This viremia may arise from latently infected reservoirs such as resting memory CD4+ T‐cells or sanctuary sites where drug penetration is suboptimal. HIV latency is established at the transcriptional level and the latent state is mediated via epigenetic modifications of the integrated promoter. This review examines in details the role played by epigenetic modifiers in the repression of HIV transcription and its reactivation. We also review existing models for HIV latency in vitro and their use as experimental systems to identify small molecules that reactivate latent HIV.
© 2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
| Authors: | Hakre, Shweta; Chavez, Leonard; Shirakawa, Kotaro; Verdin, Eric | |
| Journal: | FEMS Microbiology Reviews | |
| Volume: | 36 | |
| Issue: | 3 | |
| Year: | 2012 | |
| Pages: | 706 | |
| DOI: | 10.1111/j.1574-6976.2012.00335.x | |
| Publication date: | 01-05-2012 |
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