ArticleJournal of acquired immune deficiency syndromes (1999)2010
The histone deacetylase inhibitor ITF2357 decreases surface CXCR4 and CCR5 expression on CD4(+) T-cells and monocytes and is superior to valproic acid for latent HIV-1 expression in vitro.
Article in Journal of acquired immune deficiency syndromes (1999), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 82 citations in OpenAlex.
- Provirus activation plus CD59 blockage triggers antibody-dependent complement-mediated lysis of latently HIV-1-infected cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Substrate-Guided Development of HDAC11-Selective Inhibitors Featuring α‑Amino Amide Zinc-Binding Groups.ACS omega · 2025Article
- Isoform-Selective Versus Nonselective Histone Deacetylase Inhibitors in HIV Latency Reversal.AIDS research and human retroviruses · 2022Review
- Bryostatin-1 Decreases HIV-1 Infection and Viral Production in Human Primary Macrophages.Journal of virology · 2022Article
- Role of Histone Deacetylases in Monocyte Function in Health and Chronic Inflammatory Diseases.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Article
- Novel Histone Deacetylase Inhibitors and HIV-1 Latency-Reversing Agents Identified by Large-Scale Virtual Screening.Frontiers in pharmacology · 2020Article
- Exploring the Drug Repurposing Versatility of Valproic Acid as a Multifunctional Regulator of Innate and Adaptive Immune Cells.Journal of immunology research · 2019Review
- Neutralizing negative epigenetic regulation by HDAC5 enhances human haematopoietic stem cell homing and engraftment.Nature communications · 2018Article
- Review
- Epigenetic Metabolite Acetate Inhibits Class I/II Histone Deacetylases, Promotes Histone Acetylation, and Increases HIV-1 Integration in CD4Journal of virology · 2017Article
- Sequential treatment with 5-aza-2'-deoxycytidine and deacetylase inhibitors reactivates HIV-1.EMBO molecular medicine · 2016Article
- Impact of Chromatin on HIV Replication.Genes · 2015Review
- H3K27 Demethylation at the Proviral Promoter Sensitizes Latent HIV to the Effects of Vorinostat in Ex Vivo Cultures of Resting CD4+ T Cells.Journal of virology · 2015Article
- Specific inhibition of histone deacetylase 8 reduces gene expression and production of proinflammatory cytokines in vitro and in vivo.The Journal of biological chemistry · 2015Article
- Epigenetic control of HIV-1 post integration latency: implications for therapy.Clinical epigenetics · 2015Review
- Exploring the potential of monoclonal antibody therapeutics for HIV-1 eradication.AIDS research and human retroviruses · 2015Article
- Dilazep synergistically reactivates latent HIV-1 in latently infected cells.Molecular biology reports · 2014Article
- Effect of suberoylanilide hydroxamic acid (SAHA) administration on the residual virus pool in a model of combination antiretroviral therapy-mediated suppression in SIVmac239-infected indian rhesus macaques.Antimicrobial agents and chemotherapy · 2014Article
- The histone deacetylase inhibitor vorinostat (SAHA) increases the susceptibility of uninfected CD4+ T cells to HIV by increasing the kinetics and efficiency of postentry viral events.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
objectivesChromatin-associated repression is one mechanism that maintains HIV-1 latency. Inhibition of histone deacetylases (HDAC) reverses this repression resulting in viral expression from quiescently infected cells. Clinical studies with the HDAC inhibitor valproic acid (VPA) failed to substantially decrease the latent pool within resting CD4(+) cells. Here we compared the efficacy of ITF2357, an orally active and safe HDAC inhibitor, with VPA for HIV-1 expression from latently infected cells in vitro. We also evaluated the effect of ITF2357 on the surface expression of CXCR4 and CCR5.
methodsLatently infected cell lines were incubated with either ITF2357 or VPA and p24 levels were measured. Peripheral blood mononuclear cells of uninfected donors were treated with ITF2357 and HIV-1 coreceptors expression was assessed by flow cytometry.
resultsAt clinically relevant concentrations, ITF2357 increased p24 by 15-fold in ACH2 cells and by 9-fold in U1 cells, whereas VPA increased expression less than 2-fold. Analogues of ITF2357 primarily targeting HDAC-1 increased p24 up to 30-fold. In CD4(+) T cells treated with ITF2357, CXCR4 expression decreased by 54% (P < 0.001).
conclusionITF2357 is superior to VPA in inducing HIV-1 from latently infected cells. Safely used in humans, ITF2357 is an attractive candidate for HIV-1 clinical purging.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.