ArticleCurrent HIV research2011
Control of HIV latency by epigenetic and non-epigenetic mechanisms.
Article in Current HIV research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 99 citations in OpenAlex.
- Phosphorylation of CDK9 at Ser175 enhances HIV transcription and is a marker of activated P-TEFb in CD4(+) T lymphocytes.PLoS pathogens · 2013Trial
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- CRISPR/Cas9-Based Genome Editing: Understanding Differences in DNA Repair Pathways, Profiles, and Outcomes.International journal of molecular sciences · 2026Review
- Latent HIV Reservoirs in the Central Nervous System: Mechanisms, Barriers, and Therapeutic Approaches.ACS infectious diseases · 2026Review
- USP45-mediated deubiquitination of HIV-1 Tat regulates viral transcription and latency.Frontiers in microbiology · 2026Article
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- Cocaine-induced DNA-PK relieves RNAP II pausing by promoting TRIM28 phosphorylation.bioRxiv : the preprint server for biology · 2024Article
- Association of Toll-Like Receptor Gene Polymorphisms with Tuberculosis in HIV-Positive Participants.Epigenomes · 2023Article
- Clearance of HIV-1 or SIV reservoirs by promotion of apoptosis and inhibition of autophagy: Targeting intracellular molecules in cure-directed strategies.Journal of leukocyte biology · 2022Review
- Single-Cell Profiling of Latently SIV-Infected CD4Microbiology spectrum · 2022Article
- Heterogeneity of Latency Establishment in the Different Human CD4Journal of virology · 2022Article
- Combinatorial Use of Both Epigenetic and Non-Epigenetic Mechanisms to Efficiently Reactivate HIV Latency.International journal of molecular sciences · 2021Review
- A functional screen identifies transcriptional networks that regulate HIV-1 and HIV-2.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Challenges and Promise of Human Immunodeficiency Virus Remission.The Journal of infectious diseases · 2021Review
- Balance between Retroviral Latency and Transcription: Based on HIV Model.Pathogens (Basel, Switzerland) · 2020Review
- Review
- Epigenome-wide association scan identifies methylation sites associated with HIV infection.Epigenomics · 2020Article
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- Article
- The state of latency in microbial pathogenesis.The Journal of clinical investigation · 2020Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution.
Funding
Abstract
Intensive antiretroviral therapy successfully suppresses viral replication but is unable to eradicate the virus. HIV persists in a small number of resting memory T cells where HIV has been transcriptionally silenced. This review will focus on recent insights into the HIV transcriptional control mechanisms that provide the biochemical basis for understanding latency. There are no specific repressors of HIV transcription encoded by the virus, instead latency arises when the regulatory feedback mechanism driven by HIV Tat expression is disrupted. Small changes in transcriptional initiation, induced by epigenetic silencing, lead to profound restrictions in Tat levels and force the entry of proviruses into latency. In resting memory T cells, which carry the bulk of the latent viral pool, additional restrictions, especially the limiting cellular levels of the essential Tat cofactor P-TEFb and the transcription initiation factors NF-κB and NFAT ensure that the provirus remains silenced unless the host cell is activated. The detailed understanding of HIV transcription is providing a framework for devising new therapeutic strategies designed to purge the latent viral pool. Importantly, the recognition that there are multiple restrictions imposed on latent proviruses suggest that proviral reactivation will not be achieved when only a single reactivation step is targeted and that any optimal activation strategy will require both removal of epigenetic blocks and the activation of P-TEFb.
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What OpenQuestion holds
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.