Our data revealed that infection with both strains resulted in high expression of several antiviral genes, including IFNB, some ISGs (MX1, OAS2, and ISG15), RIG-I receptors (DDX58 and IFIH1), as well as the regulator DHX58 and the transcription factor IRF-7, which corroborated an activation of the innate immune defense as early as 3 hpi. The gene discussed is OAS2; the disease is infection.