ArticleThe Journal of biological chemistry2013
Histone deacetylase inhibitors (HDACis) that release the positive transcription elongation factor b (P-TEFb) from its inhibitory complex also activate HIV transcription.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 83 citations in OpenAlex.
- Characterization of the HIV-1 transcription profile after romidepsin administration in ART-suppressed individuals.AIDS (London, England) · 2019Trial
- Activation of HIV transcription with short-course vorinostat in HIV-infected patients on suppressive antiretroviral therapy.PLoS pathogens · 2014Trial
- Latent HIV Reservoirs in the Central Nervous System: Mechanisms, Barriers, and Therapeutic Approaches.ACS infectious diseases · 2026Review
- TARDBP as a regulator of HIV-1 assembly and infection: a review of targeting the viral capsid precursor Pr55Gag and limiting viral core entry.Cell communication and signaling : CCS · 2026Review
- HIV-1 latency reversal agent boosting is not limited by opioid use.JCI insight · 2024Article
- HIV-1 latency reversal agent boosting is not limited by opioid use.medRxiv : the preprint server for health sciences · 2024Article
- A histone deacetylase network regulates epigenetic reprogramming and viral silencing in HIV-infected cells.Cell chemical biology · 2023Article
- Potent latency reversal by Tat RNA-containing nanoparticle enables multi-omic analysis of the HIV-1 reservoir.Nature communications · 2023Article
- TRIM5α recruits HDAC1 to p50 and Sp1 and promotes H3K9 deacetylation at the HIV-1 LTR.Nature communications · 2023Article
- Microglia: The Real Foe in HIV-1-Associated Neurocognitive Disorders?Biomedicines · 2021Review
- Latency Reversing Agents: Kick and Kill of HTLV-1?International journal of molecular sciences · 2021Review
- Review
- Proteasomal Inhibition Potentiates Latent HIV Reactivation.AIDS research and human retroviruses · 2020Article
- The expression of long non-coding RNAs is associated with H3Ac and H3K4me2 changes regulated by the HDA6-LDL1/2 histone modification complex inNAR genomics and bioinformatics · 2020Article
- HSF1 inhibition attenuates HIV-1 latency reversal mediated by several candidate LRAs In Vitro and Ex Vivo.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The multifaceted nature of HIV latency.The Journal of clinical investigation · 2020Review
- Cellular Gene Modulation of HIV-Infected CD4 T Cells in Response to Serial Treatment with the Histone Deacetylase Inhibitor Vorinostat.Journal of virology · 2020Article
- P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020Review
- Bromodomain and Extraterminal Inhibition by JQ1 Produces Divergent Transcriptional Regulation of Suppressors of Cytokine Signaling Genes in Adipocytes.Endocrinology · 2020Article
- Latency-Reversing Agents Induce Differential Responses in Distinct Memory CD4 T Cell Subsets in Individuals on Antiretroviral Therapy.Cell reports · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Numerous studies have looked at the effects of histone deacetylase inhibitors (HDACis) on HIV reactivation in established transformed cell lines and primary CD4(+) T cells. However, their findings remain confusing, and differences between effects of class I- and class II-specific HDACis persist. Because no clear picture emerged, we decided to determine how HDACis reactivate HIV in transformed cell lines and primary cells. We found that neither histone H3 nor tubulin acetylation correlated with HIV reactivation in Jurkat and HeLa cells. Rather, HDACis that could reactivate HIV in chromatin or on episomal plasmids also released free positive transcription elongation factor b (P-TEFb) from its inhibitory 7SK snRNP. In resting primary CD4(+) T cells, where levels of P-TEFb are vanishingly low, the most potent HDACi, suberoylanilide hydroxyamic acid (SAHA), had minimal effects. In contrast, when these cells were treated with a PKC agonist, bryostatin 1, which increased levels of P-TEFb, then SAHA once again reactivated HIV. We conclude that HDACis, which can reactivate HIV, work via the release of free P-TEFb from the 7SK snRNP.
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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.