Compared to wild type IBV, infection with the nsp15 endoribonuclease catalytic deficient mutant, rIBV-nsp15-H238A, led to accumulation of higher levels of dsRNA, strong activation of PKR, more SGs formation, concomitantly with a higher production of IFN-β and lower viral replication. The gene discussed is IFNB1; the disease is infection.