Loading...
Control of Nipah Virus Infection in Mice by the Host Adaptors Mitochondrial Antiviral Signaling Protein (MAVS) and Myeloid Differentiation Primary Response 88 (MyD88).
Iampietro, Mathieu Aurine, Noemie Dhondt, Kevin P Dumont, Claire Pelissier, Rodolphe Spanier, Julia Vallve, Audrey Raoul, Herve Horvat, Branka
Iampietro, Mathieu
Aurine, Noemie
Dhondt, Kevin P
Dumont, Claire
Pelissier, Rodolphe
Spanier, Julia
Vallve, Audrey
Raoul, Herve
Horvat, Branka
Citations
Altmetric:
Advisors
Editors
Other Contributors
Issue Date
2019-12-19
Submitted date
Files
Loading...
corrected proof
Adobe PDF, 1.19 MB
Other Titles
Abstract
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.
Publisher
Journal
PubMed ID
PubMed Central ID
Additional Links
Embedded video
Type
Article
Language
en
Description
Series/Report no.
ISSN
1537-6613
EISSN
ISBN
ISMN
Gov't Doc #
Sponsors
License
Attribution-NonCommercial-ShareAlike 4.0 International