Antagonism of STAT1 by Nipah virus P gene products modulates disease course but not lethal outcome in the ferret model.

ABSTRACT: Nipah virus (NiV) is a pathogenic paramyxovirus and zoononis with very high human fatality rates. Previous protein over-expression studies have shown that various mutations to the common N-terminal STAT1-binding motif of the NiV P, V, and W proteins affected the STAT1-binding ability of these proteins thus interfering with he JAK/STAT pathway and reducing their ability to inhibit type-I IFN signaling, but due to differing techniques it was unclear which amino acids were most important in this interaction or what impact this had on pathogenesis in vivo. We compared all previously described mutations in parallel and found the amino acid mutation Y116E demonstrated the greatest reduction in binding to STAT1 and the greatest reduction in interferon antagonism. A similar reduction in binding an

SUBMITTER: Satterfield BA 

PROVIDER: S-EPMC6853903 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature