We then examined IRF3 phosphorylation, dimerization and nuclear translocation, three key events that determine IRF3 activation29, during viral infection and in the presence or absence of EGLN1. Remarkably, in response to SeV, VSV or HSV-1 infection, IRF3 phosphorylation and dimerization were attenuated in EGLN1−/− H1299 cells or EGLN1−/− THP-1 cells compared to EGLN1+/+ H1299 cells or EGLN1+/+ THP-1 cells (Supplementary Fig. 12b and Fig. 7d, e). This evidence concerns the gene IRF3 and viral infectious disease.