ReviewCurrent opinion in HIV and AIDS2011
The molecular biology of HIV latency: breaking and restoring the Tat-dependent transcriptional circuit.
Review in Current opinion in HIV and AIDS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 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
129 citing papers in PubMed, 179 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
- TRIP12 promotes HIV-1 replication and latency reactivation by stabilizing Tat via USP7-mediated deubiquitination.Journal of virology · 2026Article
- Latent HIV Reservoirs in the Central Nervous System: Mechanisms, Barriers, and Therapeutic Approaches.ACS infectious diseases · 2026Review
- HIV-producing resting T cells monopolize virus production, associated PANoptosis, and persistence in lymphoid tissue.bioRxiv : the preprint server for biology · 2026Article
- USP45-mediated deubiquitination of HIV-1 Tat regulates viral transcription and latency.Frontiers in microbiology · 2026Article
- Neuroinflammatory and Neurodegenerative Roles of HIV-1 Tat: A Review of Recent Evidence.Advances in experimental medicine and biology · 2026Review
- Mathematical modeling and mechanisms of HIV latency for personalized anti latency therapies.NPJ systems biology and applications · 2025Review
- Ripretinib inhibits HIV-1 transcription through modulation of PI3K-AKT-mTOR.Acta pharmacologica Sinica · 2024Article
- Monocyte to macrophage differentiation and changes in cellular redox homeostasis promote cell type-specific HIV latency reactivation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Small molecule inhibitors of transcriptional cyclin-dependent kinases impose HIV-1 latency, presenting "block and lock" treatment strategies.Antimicrobial agents and chemotherapy · 2024Article
- Article
- HIV Expression in Infected T Cell Clones.Viruses · 2024Review
- Breaking the Silence: Regulation of HIV Transcription and Latency on the Road to a Cure.Viruses · 2023Review
- Initial productive and latent HIV infections originate in vivo by infection of resting T cells.The Journal of clinical investigation · 2023Article
- The role of tunneling nanotubes during early stages of HIV infection and reactivation: implications in HIV cure.NeuroImmune pharmacology and therapeutics · 2023Review
- TRIM24 controls induction of latent HIV-1 by stimulating transcriptional elongation.Communications biology · 2023Article
- Strategies to overcome HIV drug resistance-current and future perspectives.Frontiers in microbiology · 2023Review
- Review
- T cell stimulation remodels the latently HIV-1 infected cell population by differential activation of proviral chromatin.PLoS pathogens · 2022Article
- Combined noncanonical NF-κB agonism and targeted BET bromodomain inhibition reverse HIV latency ex vivo.The Journal of clinical investigation · 2022Article
69 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
1 author at 1 institution in 1 country.
Funding
Abstract
purpose of reviewDespite the remarkable success of intensive antiretroviral drug therapy in blocking the HIV replication, the virus persists in a small number of cells in which 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. RECENT
findingsLatency arises when the regulatory feedback mechanism driven by HIV Tat expression is disrupted. Small changes in transcriptional initiation, induced by epigenetic silencing, can lead to restrictions in Tat levels and entry of proviruses into latency. In resting memory T-cells, which carry the bulk of the latent viral pool, additional restrictions limiting cellular levels of the essential Tat cofactor P-TEFb and the transcription initiation factors nuclear factor kappa B and nuclear factor of activated T cells ensure that the provirus remains silenced unless the host cell is activated. SUMMARY: Strategies to purge the latent proviral pool require nontoxic activator molecules. The multiple restrictions imposed on latent proviruses that need to be overcome suggest that proviral reactivation will not be achieved when only a single reactivation step is targeted but will require both removal of epigenetic blocks and the activation of P-TEFb. Alternatively, new inhibitors that block proviral reactivation could be developed.
Indexed as
Identifiers
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.