To test whether the MA NS1 mutations conferred increased viral protein synthesis, and whether these mutations influenced resistance of viral protein synthesis to the IFN-β-mediated anti-viral response, we evaluated the level of M1 and NS1 viral protein synthesis by pulse labelling with 35S-labeled cysteine and methionine residues during the course of infection in M1 cells (MOI = 2), both in untreated and in IFN-β primed cells that were treated with 200 U/mL mouse IFN-β for 24 hours prior to infection. Here, IFNB1 is linked to infection.