ArticlePLoS pathogens2014
Dynamics of HIV latency and reactivation in a primary CD4+ T cell model.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Transcriptome profiles of latently- and reactivated HIV-1 infected primary CD4Frontiers in immunology · 2022Pooled it
- Standard vaccines increase HIV-1 transcription during antiretroviral therapy.AIDS (London, England) · 2016Trial
- The Depsipeptide Romidepsin Reverses HIV-1 Latency In Vivo.PLoS pathogens · 2015Trial
- Network Pharmacology-Guided Identification ofInternational journal of molecular sciences · 2026Article
- HIV-1 latency reversing agents converge on phosphoregulation of nuclear protein complexes.bioRxiv : the preprint server for biology · 2025Article
- HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency.Nature microbiology · 2025Article
- Inhibition of ALKBH5 demethylase of mVirology journal · 2025Article
- Heat shock protein 90 is a chaperone regulator of HIV-1 latency.PLoS pathogens · 2025Article
- Nuclear retention of unspliced HIV-1 RNA as a reversible post-transcriptional block in latency.Nature communications · 2025Article
- The role of Tat in HIV latency and reactivation.Frontiers in immunology · 2025Review
- Review
- A macrophage-cell model of HIV latency reveals the unusual importance of the bromodomain axis.Virology journal · 2024Article
- Spontaneous HIV expression during suppressive ART is associated with the magnitude and function of HIV-specific CD4Cell host & microbe · 2023Article
- Schlafen 12 restricts HIV-1 latency reversal by a codon-usage dependent post-transcriptional block in CD4+ T cells.Communications biology · 2023Article
- Single-Cell Profiling of Latently SIV-Infected CD4Microbiology spectrum · 2022Article
- Disulfiram: A Repurposed Drug in Preclinical and Clinical Development for the Treatment of Infectious Diseases.Anti-infective agents · 2022Article
- Single-Cell Sequencing Facilitates Elucidation of HIV Immunopathogenesis: A Review of Current Literature.Frontiers in immunology · 2022Review
- HDAC inhibitors Panobinostat and Romidepsin enhanceFrontiers in immunology · 2022Article
- HIV-1 persistence in the CNS: Mechanisms of latency, pathogenesis and an update on eradication strategies.Virus research · 2021Review
- Addressing an HIV cure in LMIC.Retrovirology · 2021Review
3 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
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HIV latency is a major obstacle to curing infection. Current strategies to eradicate HIV aim at increasing transcription of the latent provirus. In the present study we observed that latently infected CD4+ T cells from HIV-infected individuals failed to produce viral particles upon ex vivo exposure to SAHA (vorinostat), despite effective inhibition of histone deacetylases. To identify steps that were not susceptible to the action of SAHA or other latency reverting agents, we used a primary CD4+ T cell model, joint host and viral RNA sequencing, and a viral-encoded reporter. This model served to investigate the characteristics of latently infected cells, the dynamics of HIV latency, and the process of reactivation induced by various stimuli. During latency, we observed persistence of viral transcripts but only limited viral translation. Similarly, the reactivating agents SAHA and disulfiram successfully increased viral transcription, but failed to effectively enhance viral translation, mirroring the ex vivo data. This study highlights the importance of post-transcriptional blocks as one mechanism leading to HIV latency that needs to be relieved in order to purge the viral reservoir.
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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.