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Journal Article
Research Support, Non-U.S. Gov't
HIV-1 reactivation induced by apicidin involves histone modification in latently infected cells.
Current HIV Research 2011 June
The existence of stable, transcriptionally silent human immunodeficiency virus (HIV) in latently infected cells represents a major obstacle to acquired immune deficiency syndrome (AIDS) therapy. Histone deacetylase (HDAC) can inhibit histone acetylation, resulting in HIV-1 provirus transcription silence. Apicidin, a widely used antiparasitic drug, exhibits antiparasitic activity by inhibiting HDAC. Using the latently infected A10.6 cell line, we describe the dose- and time-dependent manner in which Apicidin reverses HIV-1 latency. We found that Apicidin can synergize with trichostatin A (TSA) to activate HIV-1 gene expression. Chromatin immunoprecipitation (ChIP) assay further indicates that Apicidin induces HIV-1 reactivation by increasing the acetylation levels of H3 and H4 at nucleosome 1 in HIV-1 long terminal repeats (LTR). Our research reveals a potent activator for reactivating latent HIV-1 and shows promise for HIV-1 therapy.
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