We next examined the expression levels of RIG-1 and MDA-5, the RLR family members and cytosolic sensors for RNA viruses. We found that RIG-1 in particular was significantly induced up to 1280-fold, while MDA-5 was also upregulated up to 42-fold in infected pig macrophages (Fig. 8B) . We further examined the induction of RIG-1 and MDA-5 and their relevance to MAP kinases. To do this, we pre-treated the cells with inhibitors of MAP kinases. As shown in Figure 8C , the induction of RIG-1 was completely abolished by the inhibition of ERK1/2 or JNK1/2 inhibitors, and to a much lesser extent, by the p38 inhibitor, suggesting that the induction of RIG-1 was dependent on ERK1/ 2 and JNK1/2, but not as much on p38. This differentially regulated pattern of RIG-1 induction by ERK1/2, p38, and JNK1/2 was similar to the suppression of NFkB phosphorylation/activation by MAP kinases (Fig. 8A) , suggesting that the induction of RIG-1 was associated with ERK1/2 or JNK1/2 activation, but to a much lesser extent with p38. Since NFkB could be downstream activated by RIG-1/IPS-1 [29, 30] , we postulate that ERK1/2 or JNK1/2 may activate NFkB through the activation of RIG-1/IPS-1 during H1N1pdm infection in pig macrophages.