SARS coronavirus pathogenesis: host innate immune responses and viral antagonism of interferon.

Current Opinion in Virology
Allison L Totura, Ralph S Baric

Abstract

SARS-CoV is a pathogenic coronavirus that emerged from a zoonotic reservoir, leading to global dissemination of the virus. The association SARS-CoV with aberrant cytokine, chemokine, and Interferon Stimulated Gene (ISG) responses in patients provided evidence that SARS-CoV pathogenesis is at least partially controlled by innate immune signaling. Utilizing models for SARS-CoV infection, key components of innate immune signaling pathways have been identified as protective factors against SARS-CoV disease, including STAT1 and MyD88. Gene transcription signatures unique to SARS-CoV disease states have been identified, but host factors that regulate exacerbated disease phenotypes still remain largely undetermined. SARS-CoV encodes several proteins that modulate innate immune signaling through the antagonism of the induction of Interferon and by avoidance of ISG effector functions.

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Citations

Sep 18, 2013·Proceedings of the National Academy of Sciences of the United States of America·Trevor ScobeyRalph S Baric
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Methods Mentioned

BETA
nuclear translocation

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