Abstract
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.
Keywords: AIDS, apicidin, human immunodeficiency virus type 1, histone acetylation, histone deacetylase inhibitors, latent reservoirs, Cytotoxicity, Cell Culture, Cytometry Analysis, Toxicity Assay
Current HIV Research
Title: HIV-1 Reactivation Induced by Apicidin Involves Histone Modification in Latently Infected Cells
Volume: 9 Issue: 4
Author(s): Shiguan Lin, Yuhao Zhang, Hao Ying and Huanzhang Zhu
Affiliation:
Keywords: AIDS, apicidin, human immunodeficiency virus type 1, histone acetylation, histone deacetylase inhibitors, latent reservoirs, Cytotoxicity, Cell Culture, Cytometry Analysis, Toxicity Assay
Abstract: 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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Cite this article as:
Lin Shiguan, Zhang Yuhao, Ying Hao and Zhu Huanzhang, HIV-1 Reactivation Induced by Apicidin Involves Histone Modification in Latently Infected Cells, Current HIV Research 2011; 9 (4) . https://dx.doi.org/10.2174/157016211796320333
DOI https://dx.doi.org/10.2174/157016211796320333 |
Print ISSN 1570-162X |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4251 |
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Management of HIV: Management of HIV: old challenges and new needs
The aim of this thematic issue is to provide the most recent updates regarding the effective management of HIV infection. Antiretroviral therapy (ART) has significantly decreased HIV-related mortality, leading to an enhancement in the quality of life and life expectancy for people living with HIV (PLWH). Despite the numerous advancements ...read more
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