Control of Nipah Virus Infection in Mice by the Host Adaptors Mitochondrial Antiviral Signaling Protein (MAVS) and Myeloid Differentiation Primary Response 88 (MyD88).
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Authors
Iampietro, MathieuAurine, Noemie
Dhondt, Kevin P
Dumont, Claire
Pelissier, Rodolphe
Spanier, Julia
Vallve, Audrey
Raoul, Herve
Kalinke, Ulrich

Horvat, Branka
Issue Date
2019-12-19
Metadata
Show full item recordAbstract
Interferon (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.Citation
J Infect Dis. 2019 Dec 19. pii: 5680630. doi: 10.1093/infdis/jiz602.Affiliation
TWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH,Feodor-Lynen Str. 7, 30625 Hannover, Germany.Publisher
Oxford AcademicJournal
Journal of Infectious DiseasesPubMed ID
31853535Type
ArticleLanguage
enISSN
1537-6613ae974a485f413a2113503eed53cd6c53
10.1093/infdis/jiz602
Scopus Count
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- Creative Commons
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 4.0 International
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