Control of Nipah Virus Infection in Mice by the Host Adaptors Mitochondrial Antiviral Signaling Protein (MAVS) and Myeloid Differentiation Primary Response 88 (MyD88)
Iampietro M, Aurine N, Dhondt K, Dumont C, Pelissier R, Spanier J, Vallve A, Raoul H, Kalinke U, Horvat B
Published in
The Journal of infectious diseases: Volume 221, Issue Suppl 4, Page S401-S406
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 toll/interleukin-1 receptor/resistance [TIR] domain-containing adaptor-inducing IFN-β (TRIF), in the control of NiV infection in mice. These results reveal potential novel targets for antiviral intervention and help in understanding NiV immunopathogenesis.
Open in PubMedAuthors
Prof. Dr. Ulrich Kalinke
Executive Director
Dr. Julia Spanier
Postdoctoral Researcher