ArticleJournal of virology2009
Host cell factors and functions involved in vesicular stomatitis virus entry.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.
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Who cites it
140 citing papers in PubMed.
- How endosomal PIKfyve inhibition prevents viral membrane fusion and entry.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Inhibition of host N-myristoylation compromises the infectivity of SARS-CoV-2 due to Golgi-bypassing egress.Nature communications · 2026Article
- Cyclosporine A rescues the influenza virus fusion with IFITM3-expressing cells by relocating the restriction factor to intraluminal vesicles of multivesicular bodies.Journal of virology · 2026Article
- CELLISA - a cell-cell binding assay for evaluation of nanovesicle targeting proteins.bioRxiv : the preprint server for biology · 2026Article
- RT-qPCR and split-luciferase assays enable batch standardization and analysis of engineered virus-like particle transduction.Molecular therapy. Advances · 2026Article
- AP2: an indispensable host factor in virus infection.Journal of virology · 2026Review
- Optimization of the VSV-G backbone for amino terminal fusion with nanobodies allowing its specific retargeting to HER2 receptors.Molecular therapy. Oncology · 2025Article
- How endosomal PIKfyve inhibition prevents viral membrane fusion and entry.bioRxiv : the preprint server for biology · 2025Article
- The actin nucleation promoting factor WASH facilitates clathrin-independent endocytosis of human papillomaviruses.EMBO reports · 2025Article
- Beyond TFRC: The Pivotal Role of mGluR2 in Feline Calicivirus Entry and Replication.Veterinary sciences · 2025Article
- Structures of vesicular stomatitis virus glycoprotein G alone and bound to a neutralizing antibody.PLoS pathogens · 2025Article
- Adducin-1 Facilitates Influenza Virus Endosomal Trafficking and Uncoating by Regulating Branched Actin Dynamics and Myosin IIB Activity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Characterization of spike S1/S2 processing and entry pathways of lentiviral pseudoviruses bearing seasonal human coronaviruses NL63, 229E, and HKU1 spikes.Microbiology spectrum · 2025Article
- Inhibition of early EHDV2-Ibaraki infection steps in bovine cells by endosome alkalinization or ikarugamycin, but not by blockage of individual endocytic pathways.Frontiers in cellular and infection microbiology · 2025Article
- Engineering of Vesicular Stomatitis Virus (VSV) for Modulating Cell Death and Antitumor Immunity.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- Capturing intermediates and membrane remodeling in class III viral fusion.Science advances · 2024Article
- Dynamin independent endocytosis is an alternative cell entry mechanism for multiple animal viruses.PLoS pathogens · 2024Article
- Newcastle disease virus induces clathrin-mediated endocytosis to establish infection through the activation of PI3K/AKT signaling pathway by VEGFR2.Journal of virology · 2024Article
- The α-dystroglycan N-terminus is a broad-spectrum antiviral agent against SARS-CoV-2 and enveloped viruses.Antiviral research · 2024Article
80 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vesicular stomatitis virus (VSV) is an animal virus that based on electron microscopy and its dependence on acidic cellular compartments for infection is thought to enter its host cells in a clathrin-dependent manner. The exact cellular mechanism, however, is largely unknown. In this study, we characterized the entry kinetics of VSV and elucidated viral requirements for host cell factors during infection in HeLa cells. We found that endocytosis of VSV was a fast process with a half time of 2.5 to 3 min and that acid activation occurred within 1 to 2 min after internalization in early endosomes. The majority of viral particles were endocytosed in a clathrin-based, dynamin-2-dependent manner. Although associated with some of the surface-bound viruses, the classical adaptor protein complex AP-2 was not required for infection. Time-lapse microscopy revealed that the virus either entered preformed clathrin-coated pits or induced de novo formation of pits. Dynamin-2 was recruited to plasma membrane-confined virus particles. Thus, VSV can induce productive internalization by exploiting a specific combination of the clathrin-associated proteins and cellular functions.
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