ArticlePLoS pathogens2016
Transcriptomic Analysis Implicates the p53 Signaling Pathway in the Establishment of HIV-1 Latency in Central Memory CD4 T Cells in an In Vitro Model.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Transcriptome profiles of latently- and reactivated HIV-1 infected primary CD4Frontiers in immunology · 2022Pooled it
- Network Pharmacology-Guided Identification ofInternational journal of molecular sciences · 2026Article
- HIV-1 Integration Site Determines the Transcriptional Fate and Persistence of Integrated Proviruses.bioRxiv : the preprint server for biology · 2026Article
- HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency.Nature microbiology · 2025Article
- NSC95397 Is a Novel HIV-1 Latency-Reversing Agent.Viruses · 2024Article
- NSC95397 is a Novel HIV-1 Latency Reversing Agent.bioRxiv : the preprint server for biology · 2024Article
- Review
- The Role of p53 in HIV Infection.Current HIV/AIDS reports · 2023Review
- HIV Infection Elicits Differential Transcriptomic Remodeling in CD4+ T Cells with Variable Proliferative Responses to the T Cell Receptor Stimulus.Pathogens (Basel, Switzerland) · 2023Article
- A Camptothetin Analog, Topotecan, Promotes HIV Latency via Interference with HIV Transcription and RNA Splicing.Journal of virology · 2023Article
- Single-cell RNA sequencing reveals common and unique gene expression profiles in primary CD4+ T cells latently infected with HIV under different conditions.Frontiers in cellular and infection microbiology · 2023Article
- Integrated proteomics and transcriptomics analyses identify novel cell surface markers of HIV latency.Virology · 2022Article
- The Cultured TMethods in molecular biology (Clifton, N.J.) · 2022Article
- Intra- and extra-cellular environments contribute to the fate of HIV-1 infection.Cell reports · 2021Article
- Article
- CRL4-DCAF12 Ubiquitin Ligase Controls MOV10 RNA Helicase during Spermatogenesis and T Cell Activation.International journal of molecular sciences · 2021Article
- The Intact Non-Inducible Latent HIV-1 Reservoir is Established In anJournal of virology · 2021Article
- Micro RNA Targets in HIV Latency: Insights into Novel Layers of Latency Control.AIDS research and human retroviruses · 2021Article
- The Underrated Salivary Virome of Men Who Have Sex With Men Infected With HIV.Frontiers in immunology · 2021Article
- Network-Based Analysis of OMICs Data to Understand the HIV-Host Interaction.Frontiers in microbiology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The search for an HIV-1 cure has been greatly hindered by the presence of a viral reservoir that persists despite antiretroviral therapy (ART). Studies of HIV-1 latency in vivo are also complicated by the low proportion of latently infected cells in HIV-1 infected individuals. A number of models of HIV-1 latency have been developed to examine the signaling pathways and viral determinants of latency and reactivation. A primary cell model of HIV-1 latency, which incorporates the generation of primary central memory CD4 T cells (TCM), full-length virus infection (HIVNL4-3) and ART to suppress virus replication, was used to investigate the establishment of HIV latency using RNA-Seq. Initially, an investigation of host and viral gene expression in the resting and activated states of this model indicated that the resting condition was reflective of a latent state. Then, a comparison of the host transcriptome between the uninfected and latently infected conditions of this model identified 826 differentially expressed genes, many of which were related to p53 signaling. Inhibition of the transcriptional activity of p53 by pifithrin-α during HIV-1 infection reduced the ability of HIV-1 to be reactivated from its latent state by an unknown mechanism. In conclusion, this model may be used to screen latency reversing agents utilized in shock and kill approaches to cure HIV, to search for cellular markers of latency, and to understand the mechanisms by which HIV-1 establishes latency.
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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.