ReviewViruses2013
Lost in transcription: molecular mechanisms that control HIV latency.
Review in Viruses, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 64 citations in OpenAlex.
- Review
- HIV-1 Gag co-localizes with euchromatin histone marks at the nuclear periphery.Journal of virology · 2023Article
- Review
- Heterogeneity of Latency Establishment in the Different Human CD4Journal of virology · 2022Article
- Fighting HIV-1 Persistence: At the Crossroads of "Shoc-K and B-Lock".Pathogens (Basel, Switzerland) · 2021Review
- Are HIV-1-Specific Antibody Levels Potentially Useful Laboratory Markers to Estimate HIV Reservoir Size? A Review.Frontiers in immunology · 2021Review
- The Potential Contribution of Caveolin 1 to HIV Latent Infection.Pathogens (Basel, Switzerland) · 2020Review
- Article
- Genome-wide CRISPR knockout screen identifies ZNF304 as a silencer of HIV transcription that promotes viral latency.PLoS pathogens · 2020Article
- Article
- HIV-1 Proviral Transcription and Latency in the New Era.Viruses · 2020Review
- P-TEFb as A Promising Therapeutic Target.Molecules (Basel, Switzerland) · 2020Review
- Block-And-Lock Strategies to Cure HIV Infection.Viruses · 2020Review
- HIV-1 Latency and Latency Reversal: Does Subtype Matter?Viruses · 2019Review
- Fused in sarcoma silences HIV gene transcription and maintains viral latency through suppressing AFF4 gene activation.Retrovirology · 2019Article
- Cat and Mouse: HIV Transcription in Latency, Immune Evasion and Cure/Remission Strategies.Viruses · 2019Review
- The Role of Macrophages in HIV-1 Persistence and Pathogenesis.Frontiers in microbiology · 2019Review
- Zinc-Finger Nucleases Induced by HIV-1 Tat Excise HIV-1 from the Host Genome in Infected and Latently Infected Cells.Molecular therapy. Nucleic acids · 2018Article
- Article
- HIV latency in isolated patient CD4Science translational medicine · 2018Article
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 2 institutions in 2 countries.
Funding
Abstract
Highly active antiretroviral therapy (HAART) has limited the replication and spread of the human immunodeficiency virus (HIV). However, despite treatment, HIV infection persists in latently infected reservoirs, and once therapy is interrupted, viral replication rebounds quickly. Extensive efforts are being directed at eliminating these cell reservoirs. This feat can be achieved by reactivating latent HIV while administering drugs that prevent new rounds of infection and allow the immune system to clear the virus. However, current approaches to HIV eradication have not been effective. Moreover, as HIV latency is multifactorial, the significance of each of its molecular mechanisms is still under debate. Among these, transcriptional repression as a result of reduced levels and activity of the positive transcription elongation factor b (P-TEFb: CDK9/cyclin T) plays a significant role. Therefore, increasing levels of P-TEFb expression and activity is an excellent strategy to stimulate viral gene expression. This review summarizes the multiple steps that cause HIV to enter into latency. It positions the interplay between transcriptionally active and inactive host transcriptional activators and their viral partner Tat as valid targets for the development of new strategies to reactivate latent viral gene expression and eradicate HIV.
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.