ArticlePLoS pathogens2013
A36-dependent actin filament nucleation promotes release of vaccinia virus.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
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- Temporal expression classes and functions of vaccinia virus and mpox (monkeypox) virus genes.mBio · 2025Review
- MPXV: Update on Morphological and Morphogenesis Aspects Through Transmission and Scanning Electron Microscopies and 3D Reconstruction.Journal of medical virology · 2025Article
- Single-cell analysis of VACV infection reveals pathogen-driven timing of early and late phases and host-limited dynamics of virus production.PLoS pathogens · 2024Article
- Assembly and Evolution of Poxviruses.Advances in experimental medicine and biology · 2024Review
- ISG15 Is Required for the Dissemination of Vaccinia Virus Extracellular Virions.Microbiology spectrum · 2023Article
- Viral use and subversion of membrane organization and trafficking.Journal of cell science · 2021Review
- A putative WAVE regulatory complex (WRC) interacting receptor sequence (WIRS) in the cytoplasmic tail of HSV-1 gE does not function in WRC recruitment or neuronal transport.Access microbiology · 2021Article
- How Physical Factors Coordinate Virus Infection: A Perspective From Mechanobiology.Frontiers in bioengineering and biotechnology · 2021Review
- A Quantitative Live-Cell Superresolution Imaging Framework for Measuring the Mobility of Single Molecules at Sites of Virus Assembly.Pathogens (Basel, Switzerland) · 2020Article
- Partial Deletion of Glycoprotein B5R Enhances Vaccinia Virus Neutralization Escape while Preserving Oncolytic Function.Molecular therapy oncolytics · 2019Article
- Septins suppress the release of vaccinia virus from infected cells.The Journal of cell biology · 2018Article
- Loss of Actin-Based Motility Impairs Ectromelia Virus Release In Vitro but Is Not Critical to Spread In Vivo.Viruses · 2018Article
- Vaccinia virus egress mediated by virus protein A36 is reliant on the F12 protein.The Journal of general virology · 2017Article
- Divergent roles of β- and γ-actin isoforms during spread of vaccinia virus.Cytoskeleton (Hoboken, N.J.) · 2017Article
- Autographa californica Multiple Nucleopolyhedrovirus Ac34 Protein Retains Cellular Actin-Related Protein 2/3 Complex in the Nucleus by Subversion of CRM1-Dependent Nuclear Export.PLoS pathogens · 2016Article
- NPF motifs in the vaccinia virus protein A36 recruit intersectin-1 to promote Cdc42:N-WASP-mediated viral release from infected cells.Nature microbiology · 2016Article
- Analogies Between Cancer-Derived Extracellular Vesicles and Enveloped Viruses with an Emphasis on Human Breast Cancer.Current pathobiology reports · 2016Review
- Superresolution imaging of viral protein trafficking.Medical microbiology and immunology · 2015Review
- Functional comparison of herpes simplex virus 1 (HSV-1) and HSV-2 ICP27 homologs reveals a role for ICP27 in virion release.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell-to-cell transmission of vaccinia virus can be mediated by enveloped virions that remain attached to the outer surface of the cell or those released into the medium. During egress, the outer membrane of the double-enveloped virus fuses with the plasma membrane leaving extracellular virus attached to the cell surface via viral envelope proteins. Here we report that F-actin nucleation by the viral protein A36 promotes the disengagement of virus attachment and release of enveloped virus. Cells infected with the A36(YdF) virus, which has mutations at two critical tyrosine residues abrogating localised actin nucleation, displayed a 10-fold reduction in virus release. We examined A36(YdF) infected cells by transmission electron microscopy and observed that during release, virus appeared trapped in small invaginations at the plasma membrane. To further characterise the mechanism by which actin nucleation drives the dissociation of enveloped virus from the cell surface, we examined recombinant viruses by super-resolution microscopy. Fluorescently-tagged A36 was visualised at sub-viral resolution to image cell-virus attachment in mutant and parental backgrounds. We confirmed that A36(YdF) extracellular virus remained closely associated to the plasma membrane in small membrane pits. Virus-induced actin nucleation reduced the extent of association, thereby promoting the untethering of virus from the cell surface. Virus release can be enhanced via a point mutation in the luminal region of B5 (P189S), another virus envelope protein. We found that the B5(P189S) mutation led to reduced contact between extracellular virus and the host membrane during release, even in the absence of virus-induced actin nucleation. Our results posit that during release virus is tightly tethered to the host cell through interactions mediated by viral envelope proteins. Untethering of virus into the surrounding extracellular space requires these interactions be relieved, either through the force of actin nucleation or by mutations in luminal proteins that weaken these interactions.
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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.