ArticleJournal of virology2004
Vaccinia virus entry into cells is dependent on a virion surface protein encoded by the A28L gene.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 106 citations in OpenAlex.
- Structure and functional analyses of vaccinia virus J5 protein reveal distinct determinants for entry-fusion complex assembly and activation.Journal of virology · 2026Article
- Structural basis of mpox virus A30/H2 subcomplex formation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cryo-EM structure of the vaccinia virus entry fusion complex reveals a multicomponent fusion machinery.Science advances · 2026Article
- Lumpy Skin Disease Virus Pathogenesis: Viral Protein Functions and Comparative Insights from Vaccinia Virus.Animals : an open access journal from MDPI · 2025Review
- The 2.3 Å Structure of A21, a Protein Component of the Conserved Poxvirus Entry-Fusion Complex.Journal of molecular biology · 2025Article
- Temporal expression classes and functions of vaccinia virus and mpox (monkeypox) virus genes.mBio · 2025Review
- Article
- Structural and functional analyses of viral H2 protein of the vaccinia virus entry fusion complex.Journal of virology · 2023Article
- Structural and functional analysis of vaccinia viral fusion complex component protein A28 through NMR and molecular dynamic simulations.PLoS pathogens · 2023Article
- A succession of two viral lattices drives vaccinia virus assembly.PLoS biology · 2023Article
- Functional epitopes and neutralizing antibodies of vaccinia virus.Frontiers in microbiology · 2023Review
- Insights into the Organization of the Poxvirus Multicomponent Entry-Fusion Complex from Proximity Analyses in Living Infected Cells.Journal of virology · 2021Article
- Mutations Near the N Terminus of Vaccinia Virus G9 Protein Overcome Restrictions on Cell Entry and Syncytium Formation Imposed by the A56/K2 Fusion Regulatory Complex.Journal of virology · 2020Article
- Experimental Evolution To Isolate Vaccinia Virus Adaptive G9 Mutants That Overcome Membrane Fusion Inhibition via the Vaccinia Virus A56/K2 Protein Complex.Journal of virology · 2020Article
- Nanoscale polarization of the entry fusion complex of vaccinia virus drives efficient fusion.Nature microbiology · 2019Article
- A comparative review of viral entry and attachment during large and giant dsDNA virus infections.Archives of virology · 2017Review
- Membrane fusion during poxvirus entry.Seminars in cell & developmental biology · 2016Review
- Intracellular Transport of Vaccinia Virus in HeLa Cells Requires WASH-VPEF/FAM21-Retromer Complexes and Recycling Molecules Rab11 and Rab22.Journal of virology · 2015Article
- Review
- Role of the vaccinia virus O3 protein in cell entry can be fulfilled by its Sequence flexible transmembrane domain.Virology · 2013Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The A28L gene of vaccinia virus is conserved in all poxviruses and encodes a protein that is anchored to the surface of infectious intracellular mature virions (IMV) and consequently lies beneath the additional envelope of extracellular virions. A conditional lethal recombinant vaccinia virus, vA28-HAi, with an inducible A28L gene, undergoes a single round of replication in the absence of inducer, producing IMV, as well as extracellular virions with actin tails, but fails to infect neighboring cells. We show here that purified A28-deficient IMV appeared to be indistinguishable from wild-type IMV and were competent to synthesize RNA in vitro. Nevertheless, A28-deficient virions did not induce cytopathic effects, express early genes, or initiate a productive infection. Although A28-deficient IMV bound to the surface of cells, their cores did not penetrate into the cytoplasm. An associated defect in membrane fusion was demonstrated by the failure of low pH to trigger syncytium formation when cells were infected with vA28-HAi in the absence of inducer (fusion from within) or when cells were incubated with a high multiplicity of A28-deficient virions (fusion from without). The correlation between the entry block and the inability of A28-deficient virions to mediate fusion provided compelling evidence for a relationship between these events. Because repression of A28 inhibited cell-to-cell spread, which is mediated by extracellular virions, all forms of vaccinia virus regardless of their outer coat must use a common A28-dependent mechanism of cell penetration. Furthermore, since A28 is conserved, all poxviruses are likely to penetrate cells in a similar way.
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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.