ArticlePloS one2014
Selective HDAC inhibition for the disruption of latent HIV-1 infection.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 78 citations in OpenAlex.
- From Epigenetic Regulation to Protein Degradation: Emerging Strategies for Anti-Infective Drug Discovery.International journal of molecular sciences · 2026Review
- Epigenetic mechanisms of retroviral regulation: a comparative review.Epigenetics & chromatin · 2026Review
- The p400 complex promotes HIV-1 latency by suppressing viral transcription and altering the host cell state.Nucleic acids research · 2025Article
- HDAC3 as an Emerging Therapeutic Target for Alzheimer's Disease and other Neurological Disorders.Molecular neurobiology · 2025Review
- RYBP promotes HIV-1 latency through promoting H2AK119ub and decreasing H3K4me3.Cell communication and signaling : CCS · 2025Article
- Latency Reversing Agents and the Road to an HIV CurePathogens (Basel, Switzerland) · 2025Review
- The role of Tat in HIV latency and reactivation.Frontiers in immunology · 2025Review
- Transcriptional repression by HDAC3 mediates T cell exclusion fromProceedings of the National Academy of Sciences of the United States of America · 2024Article
- The histone methyltransferase SETD2 regulates HIV expression and latency.PLoS pathogens · 2024Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- A histone deacetylase network regulates epigenetic reprogramming and viral silencing in HIV-infected cells.Cell chemical biology · 2023Article
- Medicinal chemistry advances in targeting class I histone deacetylases.Exploration of targeted anti-tumor therapy · 2023Review
- Medicinal Chemistry of Anti-HIV-1 Latency Chemotherapeutics: Biotargets, Binding Modes and Structure-Activity Relationship Investigation.Molecules (Basel, Switzerland) · 2022Review
- Isoform-Selective Versus Nonselective Histone Deacetylase Inhibitors in HIV Latency Reversal.AIDS research and human retroviruses · 2022Review
- Article
- Epigenomic characterization of latent HIV infection identifies latency regulating transcription factors.PLoS pathogens · 2021Article
- Discovery of Highly Selective and Potent HDAC3 Inhibitors Based on a 2-Substituted Benzamide Zinc Binding Group.ACS medicinal chemistry letters · 2020Article
- Filgotinib suppresses HIV-1-driven gene transcription by inhibiting HIV-1 splicing and T cell activation.The Journal of clinical investigation · 2020Article
- Histone deacetylase 1 interacts with HIV-1 Integrase and modulates viral replication.Virology journal · 2019Article
- Nanotechnology approaches to eradicating HIV reservoirs.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Selective histone deacetylase (HDAC) inhibitors have emerged as a potential anti-latency therapy for persistent human immunodeficiency virus type 1 (HIV-1) infection. We utilized a combination of small molecule inhibitors and short hairpin (sh)RNA-mediated gene knockdown strategies to delineate the key HDAC(s) to be targeted for selective induction of latent HIV-1 expression. Individual depletion of HDAC3 significantly induced expression from the HIV-1 promoter in the 2D10 latency cell line model. However, depletion of HDAC1 or -2 alone or in combination did not significantly induce HIV-1 expression. Co-depletion of HDAC2 and -3 resulted in a significant increase in expression from the HIV-1 promoter. Furthermore, concurrent knockdown of HDAC1, -2, and -3 resulted in a significant increase in expression from the HIV-1 promoter. Using small molecule HDAC inhibitors of differing selectivity to ablate the residual HDAC activity that remained after (sh)RNA depletion, the effect of depletion of HDAC3 was further enhanced. Enzymatic inhibition of HDAC3 with the selective small-molecule inhibitor BRD3308 activated HIV-1 transcription in the 2D10 cell line. Furthermore, ex vivo exposure to BRD3308 induced outgrowth of HIV-1 from resting CD4+ T cells isolated from antiretroviral-treated, aviremic HIV+ patients. Taken together these findings suggest that HDAC3 is an essential target to disrupt HIV-1 latency, and inhibition of HDAC2 may also contribute to the effort to purge and eradicate latent HIV-1 infection.
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Registered trials
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.