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_3
Snippet: Using virologic and transcriptomic data, the results demonstrated distinct approaches used by each virus to interfere with the global ISG response. Differences and similarities were noted between strains within each virus family, and expression patterns were further validated by proteomic data. Finally, computational and empirical studies provided insights into conserved and novel mechanisms of ISG control. Whereas the HPAI virus actively manipul.....
Document: Using virologic and transcriptomic data, the results demonstrated distinct approaches used by each virus to interfere with the global ISG response. Differences and similarities were noted between strains within each virus family, and expression patterns were further validated by proteomic data. Finally, computational and empirical studies provided insights into conserved and novel mechanisms of ISG control. Whereas the HPAI virus actively manipulated the ISG response with up-and downregulation of ISG subsets, H1N1-09 produced strong, uniform induction. In contrast, SARS-CoV and MERS-CoV successfully delayed ISG expression until after peak viral titers were achieved. Notably, MERS-CoV also downregulated a subset of ISGs, overlapping part of the signature seen with HPAI virus. Mechanistic studies revealed that absent and delayed IFN induction was responsible for the ISG antagonism observed in the CoVs. In addition, ISG downregulation in both HPAI virus and MERS-CoV was not due to disruption of signaling but rather correlates with altered histone modification, a novel avenue to impede ISG transcription. Finally, varied antagonism of HPAI virus mutants suggested that NS1 contributes to ISG control via altered histone methylation and may impact virulence in other severe influenza virus infections. Together, the data highlight unique and conserved approaches used by disparate respiratory viral pathogens to manipulate and control the global ISG responses.
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