title: SARS coronavirus pathogenesis: host innate immune responses and viral antagonism of interferon.
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.
authors.affiliation: University of North Carolina-Chapel Hill, Department of Microbiology and Immunology, Chapel Hill, NC, USA.
authors.forename: Allison L
authors.initials: AL
authors.lastname: Totura
authors.forename: Ralph S
authors.initials: RS
authors.lastname: Baric
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D057131:Immune Evasion; D007113:Immunity, Innate; D007372:Interferons / Q000037:antagonists & inhibitors*; D045473:Severe acute respiratory syndrome-related coronavirus / Q000276:immunology / Q000472:pathogenicity*; D015398:Signal Transduction; D014774:Virulence; D037521:Virulence Factors / Q000378:metabolism*
chemical_list: D037521:Virulence Factors; D007372:Interferons