Journal
TRENDS IN MICROBIOLOGY
Volume 21, Issue 6, Pages 277-285Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.tim.2013.02.005
Keywords
HIV; latency; HDAC; HDAC inhibitors
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Funding
- CFAR Basic Science Award Program in HIV/AIDS [P30AI027763]
- NIDA Avant-Garde [1DP1 DA031126, 1R01 DA030216-01]
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Latent HIV persists in CD4(+) T cells in infected patients under antiretroviral therapy (ART). Latency is associated with transcriptional silencing of the integrated provirus and driven, at least in part, by histone deacetylases (HDACs), a family of chromatin-associated proteins that regulate histone acetylation and the accessibility of DNA to transcription factors. Remarkably, inhibition of HDACs is sufficient to reactivate a fraction of latent HIV in a variety of experimental systems. This basic observation led to the shock and kill idea that forcing the transcriptional activation of HIV might lead to virus expression, to virus- or host-induced cell death of the reactivated cells, and to the eradication of the pool of latently infected cells. Such intervention might possibly lead to a cure for HIV-infected patients. Here, we review the basic biology of HDACs and their inhibitors, the role of HDACs in HIV latency, and recent efforts to use HDAC inhibitors to reactivate latent HIV in vitro and in vivo.
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