As for antiviral IFN-b, which was robustly induced with H1N1pdm infection in swine macrophages, ERK1/2 appeared to be essential since the induction of its mRNA transcripts was virtually abolished in the presence of the ERK inhibitor (Fig. 6A ). JNK1/2 may also play a role in IFN-b induction because of its significant decrease at the earlier stage of infection (16 hrs p.i.) when 3D/4 cells were pre-treated with the JNK inhibitor. However, ERK1/2 seemed to be the primary pathway in the IFN-b induction in swine macrophages. The distinct contributions to the induction of IFN-b by ERK1/2 and JNK1/2 were also reflected in the decreased mRNA transcript levels of IFN-inducible antiviral proteins, Mx and 2959-OAS, in the presence of ERK and JNK inhibitors, respectively (Fig. 6B-C) , which is in accordance with the suppression of the IFN-b induction by these same compounds in the infected cells. Both Mx and 2959-OAS were suppressed significantly by the ERK inhibitor, but only the 