Reovirus σ1 Conformational Flexibility Modulates the Efficiency of Host Cell Attachment.


Journal

Journal of virology
ISSN: 1098-5514
Titre abrégé: J Virol
Pays: United States
ID NLM: 0113724

Informations de publication

Date de publication:
09 11 2020
Historique:
received: 09 06 2020
accepted: 09 09 2020
pubmed: 18 9 2020
medline: 5 1 2021
entrez: 17 9 2020
Statut: epublish

Résumé

Reovirus attachment protein σ1 is a trimeric molecule containing tail, body, and head domains. During infection, σ1 engages sialylated glycans and junctional adhesion molecule-A (JAM-A), triggering uptake into the endocytic compartment, where virions are proteolytically converted to infectious subvirion particles (ISVPs). Further disassembly allows σ1 release and escape of transcriptionally active reovirus cores into the cytosol. Electron microscopy has revealed a distinct conformational change in σ1 from a compact form on virions to an extended form on ISVPs. To determine the importance of σ1 conformational mobility, we used reverse genetics to introduce cysteine mutations that can cross-link σ1 by establishing disulfide bonds between structurally adjacent sites in the tail, body, and head domains. We detected phenotypic differences among the engineered viruses. A mutant with a cysteine pair in the head domain replicates with enhanced kinetics, forms large plaques, and displays increased avidity for JAM-A relative to the parental virus, mimicking properties of ISVPs. However, unlike ISVPs, particles containing cysteine mutations that cross-link the head domain uncoat and transcribe viral positive-sense RNA with kinetics similar to the parental virus and are sensitive to ammonium chloride, which blocks virion-to-ISVP conversion. Together, these data suggest that σ1 conformational flexibility modulates the efficiency of reovirus host cell attachment.

Identifiants

pubmed: 32938765
pii: JVI.01163-20
doi: 10.1128/JVI.01163-20
pmc: PMC7654274
pii:
doi:

Substances chimiques

Capsid Proteins 0
Cell Adhesion Molecules 0
Receptors, Cell Surface 0
Viral Proteins 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI118887
Pays : United States

Informations de copyright

Copyright © 2020 American Society for Microbiology.

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Auteurs

Julia R Diller (JR)

Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Sean R Halloran (SR)

Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Melanie Koehler (M)

Louvain Institute of Biomolecular Science and Technology, Université Catholique de Louvain, Ottignies-Louvain-la-Neuve, Belgium.

Rita Dos Santos Natividade (R)

Louvain Institute of Biomolecular Science and Technology, Université Catholique de Louvain, Ottignies-Louvain-la-Neuve, Belgium.

David Alsteens (D)

Louvain Institute of Biomolecular Science and Technology, Université Catholique de Louvain, Ottignies-Louvain-la-Neuve, Belgium.
Walloon Excellence in Life Sciences and Biotechnology (WELBIO), Wavre, Belgium.

Thilo Stehle (T)

Interfaculty Institute of Biochemistry, University of Tübingen, Tübingen, Germany.

Terence S Dermody (TS)

Departments of Pediatrics and Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, and Center for Microbial Pathogenesis, UPMC Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA terence.dermody@chp.edu kristen.ogden@vumc.org.

Kristen M Ogden (KM)

Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA terence.dermody@chp.edu kristen.ogden@vumc.org.
Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

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