ReviewViruses2023
Transcriptional Stochasticity as a Key Aspect of HIV-1 Latency.
Review in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Transcription of HIV-1 is heterogenous among authentic latent CD4+ T cell clones.The Journal of experimental medicine · 2026Article
- Investigating the dynamics of proviral silencing in polyclonal HIV-1 infected Jurkat cell populations.bioRxiv : the preprint server for biology · 2026Article
- RNA splicing patterns contribute to burst size variation among HIV-1-infected Jurkat cell clones.Journal of virology · 2025Article
- Stochastic gene expression in proliferating cells: Differing noise intensity in single-cell and population perspectives.PLoS computational biology · 2025Article
- Host factor Naf1 restricts HIV-1 infection of myeloid cells and compromises the capacity of dendritic cell to prime CD4Virologica Sinica · 2025Article
- Identification of molecular determinants of gene-specific bursting patterns by high-throughput imaging screens.Molecular cell · 2025Article
- Review
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- Stochastic Gene Expression in Proliferating Cells: Differing Noise Intensity in Single-Cell and Population Perspectives.bioRxiv : the preprint server for biology · 2024Article
- Identification of molecular determinants of gene-specific bursting patterns by high-throughput imaging screens.bioRxiv : the preprint server for biology · 2024Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
- Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review summarizes current advances in the role of transcriptional stochasticity in HIV-1 latency, which were possible in a large part due to the development of single-cell approaches. HIV-1 transcription proceeds in bursts of RNA production, which stem from the stochastic switching of the viral promoter between ON and OFF states. This switching is caused by random binding dynamics of transcription factors and nucleosomes to the viral promoter and occurs at several time scales from minutes to hours. Transcriptional bursts are mainly controlled by the core transcription factors TBP, SP1 and NF-κb, the chromatin status of the viral promoter and RNA polymerase II pausing. In particular, spontaneous variability in the promoter chromatin creates heterogeneity in the response to activators such as TNF-α, which is then amplified by the Tat feedback loop to generate high and low viral transcriptional states. This phenomenon is likely at the basis of the partial and stochastic response of latent T cells from HIV-1 patients to latency-reversing agents, which is a barrier for the development of shock-and-kill strategies of viral eradication. A detailed understanding of the transcriptional stochasticity of HIV-1 and the possibility to precisely model this phenomenon will be important assets to develop more effective therapeutic strategies.
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