ArticleCell reports2019
Transcriptional Circuit Fragility Influences HIV Proviral Fate.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency.Nature microbiology · 2025Article
- Mathematical modeling and mechanisms of HIV latency for personalized anti latency therapies.NPJ systems biology and applications · 2025Review
- KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025Review
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- KAP1 negatively regulates RNA polymerase II elongation kinetics to activate signal-induced transcription.Nature communications · 2024Article
- KAP1 negatively regulates RNA polymerase II elongation kinetics to activate signal-induced transcription.bioRxiv : the preprint server for biology · 2024Article
- The cell biology of HIV-1 latency and rebound.Retrovirology · 2024Review
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- TRIM24 controls induction of latent HIV-1 by stimulating transcriptional elongation.Communications biology · 2023Article
- Host Cell Redox Alterations Promote Latent HIV-1 Reactivation through Atypical Transcription Factor Cooperativity.Viruses · 2022Article
- Review
- T cell stimulation remodels the latently HIV-1 infected cell population by differential activation of proviral chromatin.PLoS pathogens · 2022Article
- KAP1/TRIM28: Transcriptional Activator and/or Repressor of Viral and Cellular Programs?Frontiers in cellular and infection microbiology · 2022Review
- Cure and Long-Term Remission Strategies.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Decoding Human Genome Regulatory Features That Influence HIV-1 Proviral Expression and Fate Through an Integrated Genomics Approach.Bioinformatics and biology insights · 2022Article
- Review
- Cleavage and Polyadenylation Specificity Factor 6 Is Required for Efficient HIV-1 Latency Reversal.mBio · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Transcriptional circuit architectures in several organisms have been evolutionarily selected to dictate precise given responses. Unlike these cellular systems, HIV is regulated through a complex circuit composed of two successive phases (host and viral), which create a positive feedback loop facilitating viral replication. However, it has long remained unclear whether both phases operate identically and to what extent the host phase influences the entire circuit. Here, we report that, although the host phase is regulated by a checkpoint whereby KAP1 mediates transcription activation, the virus evolved a minimalist system bypassing KAP1. Given the complex circuit's architecture, cell-to-cell KAP1 fluctuations impart heterogeneity in the host transcriptional responses, thus affecting the feedback loop. Mathematical modeling of a complete circuit reveals how these oscillations ultimately influence homogeneous reactivation potential of a latent virus. Thus, although HIV drives molecular innovation to fuel robust gene activation, it experiences transcriptional fragility, thereby influencing viral fate and cure efforts.
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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.