ArticlePLoS pathogens2019
Strength of T cell signaling regulates HIV-1 replication and establishment of latency.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 23 citations in OpenAlex.
- Review
- A histone deacetylase network regulates epigenetic reprogramming and viral silencing in HIV-infected cells.Cell chemical biology · 2023Article
- Lymph node dendritic cells harbor inducible replication-competent HIV despite years of suppressive ART.Cell host & microbe · 2023Article
- Upstream Stimulatory Factors Regulate HIV-1 Latency and Are Required for Robust T Cell Activation.Viruses · 2023Article
- HIV Infection Elicits Differential Transcriptomic Remodeling in CD4+ T Cells with Variable Proliferative Responses to the T Cell Receptor Stimulus.Pathogens (Basel, Switzerland) · 2023Article
- Virally Suppressed People Living with HIV Who Use Opioids Have Diminished Latency Reversal.Viruses · 2023Article
- New insights into transcription elongation control of HIV-1 latency and rebound.Trends in immunology · 2023Review
- Development of an HIV reporter virus that identifies latently infected CD4Cell reports methods · 2022Article
- Lentiviral Nef Proteins Differentially Govern the Establishment of Viral Latency.Journal of virology · 2022Article
- Intragenic proviral elements support transcription of defective HIV-1 proviruses.PLoS pathogens · 2021Article
- Epigenetic Mechanisms of HIV-1 Persistence.Vaccines · 2021Review
- A functional screen identifies transcriptional networks that regulate HIV-1 and HIV-2.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Micro RNA Targets in HIV Latency: Insights into Novel Layers of Latency Control.AIDS research and human retroviruses · 2021Article
- HIV persistence in subsets of CD4+ T cells: 50 shades of reservoirs.Seminars in immunology · 2021Review
- Targeted Chromatinization and Repression of HIV-1 Provirus Transcription with Repurposed CRISPR/Cas9.Viruses · 2020Article
- Enhanced Human Immunodeficiency Virus-1 Replication in CD4+ T Cells Derived From Individuals With Latent Mycobacterium tuberculosis Infection.The Journal of infectious diseases · 2020Article
- The multifaceted nature of HIV latency.The Journal of clinical investigation · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
A major barrier to curing HIV-1 is the long-lived latent reservoir that supports re-emergence of HIV-1 upon treatment interruption. Targeting this reservoir will require mechanistic insights into the establishment and maintenance of HIV-1 latency. Whether T cell signaling at the time of HIV-1 infection influences productive replication or latency is not fully understood. We used a panel of chimeric antigen receptors (CARs) with different ligand binding affinities to induce a range of signaling strengths to model differential T cell receptor signaling at the time of HIV-1 infection. Stimulation of T cell lines or primary CD4+ T cells expressing chimeric antigen receptors supported HIV-1 infection regardless of affinity for ligand; however, only signaling by the highest affinity receptor facilitated HIV-1 expression. Activation of chimeric antigen receptors that had intermediate and low binding affinities did not support provirus transcription, suggesting that a minimal signal is required for optimal HIV-1 expression. In addition, strong signaling at the time of infection produced a latent population that was readily inducible, whereas latent cells generated in response to weaker signals were not easily reversed. Chromatin immunoprecipitation showed HIV-1 transcription was limited by transcriptional elongation and that robust signaling decreased the presence of negative elongation factor, a pausing factor, by more than 80%. These studies demonstrate that T cell signaling influences HIV-1 infection and the establishment of different subsets of latently infected cells, which may have implications for targeting the HIV-1 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.