Author: Menachery, Vineet D.; Eisfeld, Amie J.; Schäfer, Alexandra; Josset, Laurence; Sims, Amy C.; Proll, Sean; Fan, Shufang; Li, Chengjun; Neumann, Gabriele; Tilton, Susan C.; Chang, Jean; Gralinski, Lisa E.; Long, Casey; Green, Richard; Williams, Christopher M.; Weiss, Jeffrey; Matzke, Melissa M.; Webb-Robertson, Bobbie-Jo; Schepmoes, Athena A.; Shukla, Anil K.; Metz, Thomas O.; Smith, Richard D.; Waters, Katrina M.; Katze, Michael G.; Kawaoka, Yoshihiro; Baric, Ralph S.
Title: Pathogenic Influenza Viruses and Coronaviruses Utilize Similar and Contrasting Approaches To Control Interferon-Stimulated Gene Responses Document date: 2014_5_20
ID: s3zeppze_24
Snippet: The data also lent the possibility that NS1 from other pathogenic influenza strains may mediate differential antagonism of the ISG subset in addition to interfering with host recognition. Metaanalysis of NS1 from 1918 H1N1 and a seasonal influenza virus supports this possibility; while derived from Calu3 cells, the expanded ISG list demonstrated that control was altered between virulent and avirulent strains based on NS1, and the data indicated t.....
Document: The data also lent the possibility that NS1 from other pathogenic influenza strains may mediate differential antagonism of the ISG subset in addition to interfering with host recognition. Metaanalysis of NS1 from 1918 H1N1 and a seasonal influenza virus supports this possibility; while derived from Calu3 cells, the expanded ISG list demonstrated that control was altered between virulent and avirulent strains based on NS1, and the data indicated that the directions of expression changes were not uniformly in favor of the more virulent strain. Variant responses in viruses encoding different NS1 genes imply the existence of categories of NS1 genes that may target different aspects of the host immune response. This fact, coupled with highly species-specific virulence determinants (48, 49) , suggests that NS1 genes may circulate and contribute to species-specific severe disease outcomes, perhaps by coordinating unique patterns of histone modification that regulate the ISG in addition to standard IFN pathway antagonism. Importantly, exploring the global mechanism of ISG manipulation by NS1 genes within the context of infection, in addition to transfection-based approaches, will provide significant insights into disease severity across different hosts, tissues, and species.
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