ArticleVirology2007
Thermostabilizing mutations in reovirus outer-capsid protein mu1 selected by heat inactivation of infectious subvirion particles.
Article in Virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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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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
24 citing papers in PubMed, 34 citations in OpenAlex.
- Early Events in Reovirus Infection Influence Induction of Innate Immune Response.Journal of virology · 2022Article
- Control of Capsid Transformations during Reovirus Entry.Viruses · 2021Review
- Reovirus Core Proteins λ1 and σ2 Promote Stability of Disassembly Intermediates and Influence Early Replication Events.Journal of virology · 2020Article
- Selection and Characterization of a Reovirus Mutant with Increased Thermostability.Journal of virology · 2019Article
- Components of the Reovirus Capsid Differentially Contribute to Stability.Journal of virology · 2019Article
- The Loop Formed by Residues 340 to 343 of Reovirus μ1 Controls Entry-Related Conformational Changes.Journal of virology · 2017Article
- Reovirus μ1 Protein Affects Infectivity by Altering Virus-Receptor Interactions.Journal of virology · 2016Article
- Article
- PI3K/Akt/p53 pathway inhibits reovirus infection.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2015Article
- Article
- Blocking the PI3K/AKT pathway enhances mammalian reovirus replication by repressing IFN-stimulated genes.Frontiers in microbiology · 2015Article
- The μ1 72-96 loop controls conformational transitions during reovirus cell entry.Journal of virology · 2013Article
- Interferon-inducible transmembrane protein 3 (IFITM3) restricts reovirus cell entry.The Journal of biological chemistry · 2013Article
- Optimum length and flexibility of reovirus attachment protein σ1 are required for efficient viral infection.Journal of virology · 2012Article
- Recruitment of cellular clathrin to viral factories and disruption of clathrin-dependent trafficking.Traffic (Copenhagen, Denmark) · 2011Article
- Determinants of strain-specific differences in efficiency of reovirus entry.Journal of virology · 2010Article
- Article
- 3.3 A cryo-EM structure of a nonenveloped virus reveals a priming mechanism for cell entry.Cell · 2010Article
- From touchdown to transcription: the reovirus cell entry pathway.Current topics in microbiology and immunology · 2010Review
- Requirements for the formation of membrane pores by the reovirus myristoylated micro1N peptide.Journal of virology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The 76-kDa mu1 protein of nonfusogenic mammalian reovirus is a major component of the virion outer capsid, which contains 200 mu1 trimers arranged in an incomplete T=13 lattice. In virions, mu1 is largely covered by a second major outer-capsid protein, sigma3, which limits mu1 conformational mobility. In infectious subvirion particles, from which sigma3 has been removed, mu1 is broadly exposed on the surface and can be promoted to rearrange into a protease-sensitive and hydrophobic conformer, leading to membrane perforation or penetration. In this study, mutants that resisted loss of infectivity upon heat inactivation (heat-resistant mutants) were selected from infectious subvirion particles of reovirus strains Type 1 Lang and Type 3 Dearing. All of the mutants were found to have mutations in mu1, and the heat-resistance phenotype was mapped to mu1 by both recoating and reassortant genetics. Heat-resistant mutants were also resistant to rearrangement to the protease-sensitive conformer of mu1, suggesting that heat inactivation is associated with mu1 rearrangement, consistent with published results. Rate constants of heat inactivation were determined, and the dependence of inactivation rate on temperature was consistent with the Arrhenius relationship. The Gibbs free energy of activation was calculated with reference to transition-state theory and was found to be correlated with the degree of heat resistance in each of the analyzed mutants. The mutations are located in upper portions of the mu1 trimer, near intersubunit contacts either within or between trimers in the viral outer capsid. We propose that the mutants stabilize the outer capsid by interfering with unwinding of the mu1 trimer.
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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.