Together with past studies using other viruses, including IAV and Coxsackievirus B3, or sterile virus-like stimulation with poly I:C, this study indicates that PAR2 expression and activation contributes to viral infection-associated pathology by enhancing proinflammatory TLR3-NFκB responses and reducing antiviral TLR3-IFNβ responses as first suggested first by Nhu et al. The gene discussed is NFKB1; the disease is viral infectious disease.