Purpose of review: A reservoir of latently infected cells remains in HIV-infected patients treated with highly active antiretroviral therapy treatment. Persistence of HIV in this latent reservoir has prevented full viral eradication. In order to understand and develop rational therapeutics to flush out HIV latency, the molecular mechanisms governing the phenomena of HIV latency need to be understood. Several mechanisms have been proposed to explain HIV latency.
Recent findings: Epigenetic regulation of the HIV promoter in the 5′ long terminal repeat of HIV-1 via histone protein modifications and the presence of inhibitory nucleosomes play a critical role in the establishment, maintenance, and reactivation of HIV latency. Recent reports have shed further light on how HIV latency might be epigenetically regulated. In this review, we discuss how these recent reports broaden our understanding of how HIV latency is regulated. Here, we review how histone modifications and chromatin remodeling affect the transcriptional activity of the HIV promoter in the context of HIV latency.
Summary: These new epigenetic regulators of HIV latency pose as potential interesting candidates for therapeutics against HIV latency.
aGladstone Institute of Virology and Immunology, USA
bDepartment of Medicine, University of California, San Francisco, San Francisco, California, USA
Correspondence to Eric Verdin, Gladstone Institute of Virology and Immunology, San Francisco, 1650 Owens Street, San Francisco, CA 94158-2261, USA Tel: +1 415 734 4808; fax: +1 415 355 0855; e-mail: firstname.lastname@example.org