ArticleJournal of virology2020
Experimental Evolution To Isolate Vaccinia Virus Adaptive G9 Mutants That Overcome Membrane Fusion Inhibition via the Vaccinia Virus A56/K2 Protein Complex.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 7 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
- Immunogenicity of poxvirus A16/G9 entry-fusion subcomplex and its restriction by A56/K2 protein informs vaccine design.Nature microbiology · 2026Article
- Structural Insights into the Impact of the M142I Mutation in Monkeypox Virus G9 Protein on Subcomplex Formation Revealed by AlphaFold 3 Modeling.Molecules (Basel, Switzerland) · 2026Article
- Cryo-EM structure of the vaccinia virus entry fusion complex reveals a multicomponent fusion machinery.Science advances · 2026Article
- Structural dissection of vaccinia G9 identifies residues essential for membrane fusion and complex assembly.Journal of virology · 2025Article
- Structural dissection of vaccinia G9 identifies residues essential for membrane fusion and complex assembly.Journal of virology · 2025Article
- Structural and functional analyses of viral H2 protein of the vaccinia virus entry fusion complex.Journal of virology · 2023Article
- 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
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For cell entry, vaccinia virus requires fusion with the host membrane via a viral fusion complex of 11 proteins, but the mechanism remains unclear. It was shown previously that the viral proteins A56 and K2 are expressed on infected cells to prevent superinfection by extracellular vaccinia virus through binding to two components of the viral fusion complex (G9 and A16), thereby inhibiting membrane fusion. To investigate how the A56/K2 complex inhibits membrane fusion, we performed experimental evolutionary analyses by repeatedly passaging vaccinia virus in HeLa cells overexpressing the A56 and K2 proteins to isolate adaptive mutant viruses. Genome sequencing of adaptive mutants revealed that they had accumulated a unique G9R open reading frame (ORF) mutation, resulting in a single His44Tyr amino acid change. We engineered a recombinant vaccinia virus to express the G9
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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.