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A single mutation in the mammalian orthoreovirus S1 gene is responsible for increased interferon sensitivity in a virus mutant selected in Vero cells

dc.contributor.authorLanoie, Delphine
dc.contributor.authorCôté, Stéphanie
dc.contributor.authorDegeorges, Emmanuelle
dc.contributor.authorLemay, Guy
dc.date.accessioned2019-01-03T17:29:37Z
dc.date.availableMONTHS_WITHHELD:12fr
dc.date.available2019-01-03T17:29:37Z
dc.date.issued2018-12-19
dc.identifier.urihttp://hdl.handle.net/1866/21217
dc.publisherElsevierfr
dc.subjectReovirusfr
dc.subjectInterferonfr
dc.subjectReverse geneticsfr
dc.titleA single mutation in the mammalian orthoreovirus S1 gene is responsible for increased interferon sensitivity in a virus mutant selected in Vero cellsfr
dc.typeArticlefr
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Département de microbiologie, infectiologie et immunologiefr
dc.identifier.doi10.1016/j.virol.2018.12.010
dcterms.abstractIn a previous study, a mammalian orthoreovirus mutant was isolated based on its increased ability to infect interferon-defective Vero cells and was referred to as Vero-cellsadapted virus (VeroAV). This virus exhibits reduced ability to resist the antiviral effect of interferon. In the present study, the complete genome sequence of VeroAV was first determined. Reverse genetics was then used to identify a unique mutation on the S1 gene, overlapping the σ1 and σ1s reading frame, resulting in increased sensitivity to interferon. A virus lacking σ1s expression consecutive to mutation of its initiation codon was then shown to exhibit a further increase in sensitivity to interferon, supporting the idea that σ1s is the viral protein responsible. This identification of a new determinant of reovirus sensitivity to interferon gives credentials to the idea that multiple reovirus genes are responsible for the level of interferon induction and susceptibility to the interferon-induced antiviral activities.fr
dcterms.alternativeReovirus interferon sensitivityfr
dcterms.bibliographicCitationVirology ; vol. 528, p. 73-79fr
dcterms.isPartOfurn:ISSN:0042-6822fr
dcterms.languageengfr
UdeM.ReferenceFournieParDeposantdoi: 10.1016/j.virol.2018.12.010fr
UdeM.VersionRioxxVersion acceptée / Accepted Manuscriptfr


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