ArticleCell2015
A hardwired HIV latency program.
Article in Cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04263207 (Observational Study for the Evaluation of the Role of HIV-1 Tat Protein and Anti-Tat Immune Response in Peripheral Blood HIV Reservoir Dynamics), which is not on this map. Cited by 159 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.
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.
Observational Study for the Evaluation of the Role of HIV-1 Tat Protein and Anti-Tat Immune Response in Peripheral Blood HIV Reservoir Dynamics
Who cites it
159 citing papers in PubMed, 241 citations in OpenAlex.
- Cell heterogeneity contributes to the variable response of HIV-1 to latency-reversing agents.Science advances · 2026Article
- Integrating zero-inflation correction and transcriptional kinetics for single-cell transcriptomic analysis.PLoS computational biology · 2026Article
- Using the simple telegraph model to decipher transcriptional burst regulation across genome-wide data.iScience · 2026Article
- Is the molecular microenvironment of the latent HIV reservoir predictable using deep learning approaches?Journal of virology · 2026Review
- Limitations of inferring antiviral efficacy of interfering particles from observational natural histories.bioRxiv : the preprint server for biology · 2026Article
- Review
- Tools to Quantify and Characterize the Persistent Reservoir in People with HIV-1: Focus on Non-B Subtypes.Viruses · 2026Review
- IBA-1Research square · 2026Article
- The human chromatin remodeling complex p400 restricts HIV-1 transcription in a Tat-dependent manner.Nucleic acids research · 2025Article
- The RNA-binding protein RBM39 scaffolds an m⁶A-dependent RNA decay complex that destabilizes Tat transcripts and restricts HIV-1 reactivation.PLoS biology · 2025Article
- HIV-induced T cell quiescence and the origins of viral latency.Nature immunology · 2025Article
- 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
- Human chromatin remodelers regulating HIV-1 transcription: a target for small molecule inhibitors.Epigenetics & chromatin · 2025Review
- FBXO45 restricts HIV-1 replication by inducing SQSTM1/p62-mediated autophagic degradation of Tat.Journal of virology · 2025Article
- Quantifying cell fate change under different stochastic gene activation frameworks.Quantitative biology (Beijing, China) · 2025Article
- The influence of HIV sense and antisense transcripts on stochastic HIV transcription and reactivation.Computational and structural biotechnology journal · 2025Article
- The role of Tat in HIV latency and reactivation.Frontiers in immunology · 2025Review
- HIV Tat as a latency reversing agent: turning the tables on viral persistence.Frontiers in immunology · 2025Review
- Variation in HIV-1 Tat activity is a key determinant in the establishment of latent infection.JCI insight · 2024Article
99 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
5 authors at 3 institutions in 1 country.
Funding
Abstract
Biological circuits can be controlled by two general schemes: environmental sensing or autonomous programs. For viruses such as HIV, the prevailing hypothesis is that latent infection is controlled by cellular state (i.e., environment), with latency simply an epiphenomenon of infected cells transitioning from an activated to resting state. However, we find that HIV expression persists despite the activated-to-resting cellular transition. Mathematical modeling indicates that HIV's Tat positive-feedback circuitry enables this persistence and strongly controls latency. To overcome the inherent crosstalk between viral circuitry and cellular activation and to directly test this hypothesis, we synthetically decouple viral dependence on cellular environment from viral transcription. These circuits enable control of viral transcription without cellular activation and show that Tat feedback is sufficient to regulate latency independent of cellular activation. Overall, synthetic reconstruction demonstrates that a largely autonomous, viral-encoded program underlies HIV latency—potentially explaining why cell-targeted latency-reversing agents exhibit incomplete penetrance.
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.