ArticleViruses2014
Evidence showing that tetraspanins inhibit HIV-1-induced cell-cell fusion at a post-hemifusion stage.
Article in Viruses, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- How Do Cancer Cells Fuse and Why?Advances in experimental medicine and biology · 2026Review
- Lack of involvement of CD63 and CD9 tetraspanins in the extracellular vesicle content delivery process.Communications biology · 2023Article
- Endocytosed HIV-1 Envelope Glycoprotein Traffics to Rab14Journal of virology · 2022Article
- Rab3a, a small GTP-binding protein, is required for the stabilization of the murine leukaemia virus Gag protein.Small GTPases · 2022Article
- The large extracellular loop of CD63 interacts with gp41 of HIV-1 and is essential for establishing the virological synapse.Scientific reports · 2021Article
- Cell Fusion-Related Proteins and Signaling Pathways, and Their Roles in the Development and Progression of Cancer.Frontiers in cell and developmental biology · 2021Review
- Calcineurin phosphatase activity regulates Varicella-Zoster Virus induced cell-cell fusion.PLoS pathogens · 2020Article
- Tetraspanins are involved in Burkholderia pseudomallei-induced cell-to-cell fusion of phagocytic and non-phagocytic cells.Scientific reports · 2020Article
- A role for tetraspanin proteins in regulating fusion induced by Burkholderia thailandensis.Medical microbiology and immunology · 2020Article
- Article
- Tetraspanins: Architects of Viral Entry and Exit Platforms.Journal of virology · 2019Review
- Meeting Review: 2018 International Workshop on Structure and Function of the Lentiviral gp41 Cytoplasmic Tail.Viruses · 2018Article
- HIV-1 adaptation studies reveal a novel Env-mediated homeostasis mechanism for evading lethal hypermutation by APOBEC3G.PLoS pathogens · 2018Article
- CD9 Tetraspanin: A New Pathway for the Regulation of Inflammation?Frontiers in immunology · 2018Review
- More than meets the I: the diverse antiviral and cellular functions of interferon-induced transmembrane proteins.Retrovirology · 2017Review
- Review
- They Might Be Giants: Does Syncytium Formation Sink or Spread HIV Infection?PLoS pathogens · 2017Review
- Remodeling of the Host Cell Plasma Membrane by HIV-1 Nef and Vpu: A Strategy to Ensure Viral Fitness and Persistence.Viruses · 2016Review
- Coronavirus and influenza virus proteolytic priming takes place in tetraspanin-enriched membrane microdomains.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) transmission takes place primarily through cell-cell contacts known as virological synapses. Formation of these transient adhesions between infected and uninfected cells can lead to transmission of viral particles followed by separation of the cells. Alternatively, the cells can fuse, thus forming a syncytium. Tetraspanins, small scaffolding proteins that are enriched in HIV-1 virions and actively recruited to viral assembly sites, have been found to negatively regulate HIV-1 Env-induced cell-cell fusion. How these transmembrane proteins inhibit membrane fusion, however, is currently not known. As a first step towards elucidating the mechanism of fusion repression by tetraspanins, e.g., CD9 and CD63, we sought to identify the stage of the fusion process during which they operate. Using a chemical epistasis approach, four fusion inhibitors were employed in tandem with CD9 overexpression. Cells overexpressing CD9 were found to be sensitized to inhibitors targeting the pre-hairpin and hemifusion intermediates, while they were desensitized to an inhibitor of the pore expansion stage. Together with the results of a microscopy-based dye transfer assay, which revealed CD9- and CD63-induced hemifusion arrest, our investigations strongly suggest that tetraspanins block HIV-1-induced cell-cell fusion at the transition from hemifusion to pore opening.
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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.