Since both IRF3 and SVCV-P drive TBK1 phase separation, with IRF3 facilitating IFN production and SVCV-P inhibiting it by disrupting IRF3-TBK1 phase separation, we hypothesized that during SVCV infection, IRF3-TBK1 and SVCV-P-TBK1 droplets might interact and remodel into a new phase-separated state. This evidence concerns the gene IRF3 and infection.