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dc.contributor.authorIampietro, Mathieu
dc.contributor.authorAurine, Noemie
dc.contributor.authorDhondt, Kevin P
dc.contributor.authorDumont, Claire
dc.contributor.authorPelissier, Rodolphe
dc.contributor.authorSpanier, Julia
dc.contributor.authorVallve, Audrey
dc.contributor.authorRaoul, Herve
dc.contributor.authorKalinke, Ulrich
dc.contributor.authorHorvat, Branka
dc.date.accessioned2020-02-03T12:15:35Z
dc.date.available2020-02-03T12:15:35Z
dc.date.issued2019-12-19
dc.identifier.citationJ Infect Dis. 2019 Dec 19. pii: 5680630. doi: 10.1093/infdis/jiz602.en_US
dc.identifier.issn1537-6613
dc.identifier.pmid31853535
dc.identifier.doi10.1093/infdis/jiz602
dc.identifier.urihttp://hdl.handle.net/10033/622115
dc.description.abstractInterferon (IFN) type I plays a critical role in the protection of mice from lethal Nipah virus (NiV) infection, but mechanisms responsible for IFN-I induction remain unknown. In the current study, we demonstrated the critical role of the mitochondrial antiviral signaling protein signaling pathway in IFN-I production and NiV replication in murine embryonic fibroblasts in vitro, and the redundant but essential roles of both mitochondrial antiviral signaling protein and myeloid differentiation primary response 88 adaptors, but not TRIF (Toll/Interleukin-1 receptor/Resistance [TIR] domain-containing adaptor-inducing IFN-β), in the control of NiV infection in mice. These results reveal potential novel targets for antiviral intervention and help in understanding NiV immunopathogenesis.en_US
dc.language.isoenen_US
dc.publisherOxford Academicen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectMAVSen_US
dc.subjectMyD88en_US
dc.subjectNipah virusen_US
dc.subjectTLRen_US
dc.subjectTRIFen_US
dc.subjectinnate immunityen_US
dc.subjectinterferonen_US
dc.subjectmiceen_US
dc.titleControl of Nipah Virus Infection in Mice by the Host Adaptors Mitochondrial Antiviral Signaling Protein (MAVS) and Myeloid Differentiation Primary Response 88 (MyD88).en_US
dc.typeArticleen_US
dc.contributor.departmentTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH,Feodor-Lynen Str. 7, 30625 Hannover, Germany.en_US
dc.identifier.journalJournal of Infectious Diseasesen_US
refterms.dateFOA2020-02-03T12:15:35Z
dc.source.journaltitleThe Journal of infectious diseases


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