The resulting decrease in IFN production is not a result of FMDV infection causing inhibition of NF-κB translocation to the nucleus, reductions in NF-κB mRNA transcription, or a result of widespread degradation of nuclear proteins, but instead is a consequence of decreases in the nuclear levels of the p65/RelA protein subunit of NF-κB, as has also been observed during enterovirus infection. This evidence concerns the gene NFKB1 and enterovirus infectious disease.