ArticleCell reports2017
HIV-1 Activates T Cell Signaling Independently of Antigen to Drive Viral Spread.
Article in Cell reports, 2017. 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- The Activation State of CD4 T Cells Alters Cellular Peptidase Activities, HIV Antigen Processing, and MHC Class I Presentation in a Sequence-Dependent Manner.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Review
- HIV Nef disrupts Lck signaling by inducing aberrant phosphorylation of its substrates.ImmunoHorizons · 2025Article
- Optimization of a lentivirus-mediated gene therapy targeting HIV-1 RNA to eliminate HIV-1-infected cells.Molecular therapy. Nucleic acids · 2024Article
- HIV-1 virological synapse formation enhances infection spread by dysregulating Aurora Kinase B.PLoS pathogens · 2023Article
- Article
- The alphavirus nonstructural protein 2 NTPase induces a host translational shut-off through phosphorylation of eEF2 via cAMP-PKA-eEF2K signaling.PLoS pathogens · 2023Article
- Nef enhances HIV-1 replication and infectivity independently of SERINC5 in CEM T cells.Virology · 2023Article
- A cellular trafficking signal in the SIV envelope protein cytoplasmic domain is strongly selected for in pathogenic infection.PLoS pathogens · 2022Article
- HIV-1 Vpr drives a tissue residency-like phenotype during selective infection of resting memory T cells.Cell reports · 2022Article
- HIV-1 Entry and Prospects for Protecting against Infection.Microorganisms · 2021Review
- HIV-Captured DCs Regulate T Cell Migration and Cell-Cell Contact Dynamics to Enhance Viral Spread.iScience · 2020Article
- A biophysical perspective on receptor-mediated virus entry with a focus on HIV.Biochimica et biophysica acta. Biomembranes · 2020Review
- HIV Reactivation in Latently Infected Cells With Virological Synapse-Like Cell Contact.Viruses · 2020Article
- Loss of Nef-mediated CD3 down-regulation in the HIV-1 lineage increases viral infectivity and spread.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Interference with HIV infection of the first cell is essential for viral clearance at sub-optimal levels of drug inhibition.PLoS computational biology · 2020Article
- Article
- HIV Infection Stabilizes Macrophage-T Cell Interactions To Promote Cell-Cell HIV Spread.Journal of virology · 2019Article
- Mechanisms of HIV-1 cell-to-cell transmission and the establishment of the latent reservoir.Virus research · 2019Review
- Meeting Review: 2018 International Workshop on Structure and Function of the Lentiviral gp41 Cytoplasmic Tail.Viruses · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
HIV-1 spreads between CD4 T cells most efficiently through virus-induced cell-cell contacts. To test whether this process potentiates viral spread by activating signaling pathways, we developed an approach to analyze the phosphoproteome in infected and uninfected mixed-population T cells using differential metabolic labeling and mass spectrometry. We discovered HIV-1-induced activation of signaling networks during viral spread encompassing over 200 cellular proteins. Strikingly, pathways downstream of the T cell receptor were the most significantly activated, despite the absence of canonical antigen-dependent stimulation. The importance of this pathway was demonstrated by the depletion of proteins, and we show that HIV-1 Env-mediated cell-cell contact, the T cell receptor, and the Src kinase Lck were essential for signaling-dependent enhancement of viral dissemination. This study demonstrates that manipulation of signaling at immune cell contacts by HIV-1 is essential for promoting virus replication and defines a paradigm for antigen-independent T cell signaling.
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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.