Figure 5G shows that the ADV-GFP infection-induced interaction between KPNA2 and KPNA4 with IRF3 was strong at 16 hpi, at which point the phosphorylation of IRF3 was augmented (later time points were not tested). Next, we used an endogenous competition binding assay using PAMs that were transiently transfected with DP96R or empty vector, followed by infection with ADV-GFP. As the interaction between DP96R and IRF3 increased, the interaction between IRF3 and KPNA2 or KPNA4 decreased (Figure 5H). This evidence concerns the gene IRF3 and infection.