ArticleThe Journal of general virology2012
Protein B5 is required on extracellular enveloped vaccinia virus for repulsion of superinfecting virions.
Article in The Journal of general virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Temporal expression classes and functions of vaccinia virus and mpox (monkeypox) virus genes.mBio · 2025Review
- Comparative Analysis of 2022 Outbreak MPXV and Previous Clade II MPXV.Journal of medical virology · 2024Article
- Enhanced Immune Responses in Mice by Combining the Mpox Virus B6R-Protein and Aluminum Hydroxide-CpG Vaccine Adjuvants.Vaccines · 2024Article
- Two noncompeting human neutralizing antibodies targeting MPXV B6 show protective effects against orthopoxvirus infections.Nature communications · 2024Article
- ISG15 Is Required for the Dissemination of Vaccinia Virus Extracellular Virions.Microbiology spectrum · 2023Article
- Article
- Article
- Host Src controls gallid alpha herpesvirus 1 intercellular spread in a cellular fatty acid metabolism-dependent manner.Virology · 2019Article
- Partial Deletion of Glycoprotein B5R Enhances Vaccinia Virus Neutralization Escape while Preserving Oncolytic Function.Molecular therapy oncolytics · 2019Article
- Vaccinia virus-mediated cancer immunotherapy: cancer vaccines and oncolytics.Journal for immunotherapy of cancer · 2019Review
- Exploitation of Cytoskeletal Networks during Early Viral Infection.Trends in microbiology · 2019Review
- Loss of Actin-Based Motility Impairs Ectromelia Virus Release In Vitro but Is Not Critical to Spread In Vivo.Viruses · 2018Article
- Combined Proteomics/Genomics Approach Reveals Proteomic Changes of Mature Virions as a Novel Poxvirus Adaptation Mechanism.Viruses · 2017Article
- Tagging of the vaccinia virus protein F13 with mCherry causes aberrant virion morphogenesis.The Journal of general virology · 2017Article
- Vaccinia virus egress mediated by virus protein A36 is reliant on the F12 protein.The Journal of general virology · 2017Article
- Review
- Vaccinia virus protein complex F12/E2 interacts with kinesin light chain isoform 2 to engage the kinesin-1 motor complex.PLoS pathogens · 2015Article
- Arp2/3-mediated actin-based motility: a tail of pathogen abuse.Cell host & microbe · 2013Review
- A36-dependent actin filament nucleation promotes release of vaccinia virus.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
Abstract
Vaccinia virus (VACV) spreads across cell monolayers fourfold faster than predicted from its replication kinetics. Early after infection, infected cells repulse some superinfecting extracellular enveloped virus (EEV) particles by the formation of actin tails from the cell surface, thereby causing accelerated spread to uninfected cells. This strategy requires the expression of two viral proteins, A33 and A36, on the surface of infected cells and upon contact with EEV this complex induces actin polymerization. Here we have studied this phenomenon further and investigated whether A33 and A36 expression in cell lines causes an increase in VACV plaque size, whether these proteins are able to block superinfection by EEV, and which protein(s) on the EEV surface are required to initiate the formation of actin tails from infected cells. Data presented show that VACV plaque size was not increased by expression of A33 and A36, and these proteins did not block entry of the majority of EEV binding to these cells. In contrast, expression of proteins A56 and K2 inhibited entry of both EEV and intracellular mature virus. Lastly, VACV protein B5 was required on EEV to induce the formation of actin tails at the surface of cells expressing A33 and A36, and B5 short consensus repeat 4 is critical for this induction.
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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.