Together, these results show that the antiviral signalling that leads to IRF3 nuclear translocation is the rate-limiting step in antiviral gene expression, that IFIT1 and IFNB1 are associated with different levels of IRF3 nuclear translocation and, importantly, that differential IRF3 activation in response to infection probably explains the heterogeneity in transcriptional response to viral infection. This evidence concerns the gene IFNB1 and viral infectious disease.