It has been shown the PRRSV can trigger the activation of IRF-3 as well as induce IFN production at 24 h post infection but the activities are much lower than those triggered by Poly(I:C) and PRRSV nsp1 antagonizes IFN production through the TLR3 and RIG-I pathways and down-regulates the protein level of IRF-3 [58]. This evidence concerns the gene IFNA1 and infection.