SARS Coronavirus Pathogenesis: Host Innate Immune Responses and Viral Antagonism of Interferon

Overview

Journal Curr Opin Virol

Publisher Elsevier

Specialty Microbiology

Date 2012 May 11

PMID 22572391

Citations 262

Authors

Allison L Totura

Ralph S Baric

Affiliations

Soon will be listed here.

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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