IRF3 and infection: In the present study, we aim to (1) evaluate whether there are differences in rhinovirus 16 (RV 16) replication rates between healthy subjects and patients with CRSwNP; (2) determine whether the production of anti-viral interferons in cells infected with RV 16 is deficient in patients with CRSwNP; and (3) investigate whether the expression of pattern recognition receptors, phosphorylated NF-κB and IRF3, key signaling molecules implicated in RV-induced anti-viral interferons, is deficient in patients with CRSwNP after RV 16 infection and poly (I:C) treatment.