期刊
JOURNAL OF INFECTIOUS DISEASES
卷 221, 期 -, 页码 S401-S406出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiz602
关键词
Nipah virus; innate immunity; mice; MAVS; MyD88; TRIF; TLR; interferon
资金
- LabEx ECOFECT of Lyon University, within the program Investissements d'Avenir [ANR-09-MIEN-018-01, ANR-ASTRID-2011, ANR-11-LABX-0048, ANR-11-IDEX-0007]
- Aviesan Sino-French agreement on Nipah virus study
- Deutsche Forschungsgemeinschaft (Joint French-German Project cGAS-VAC) [406922110]
- DGA
- INSERM
- [ANR-18-CE11-0014-02]
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 toll/interleukin-1 receptor/resistance [TIR] domain-containing adaptor-inducing IFN-beta (TRIF), in the control of NiV infection in mice. These results reveal potential novel targets for antiviral intervention and help in understanding NiV immunopathogenesis.
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