HSV-1 synthesizes the E3 ubiquitin ligase-infected cell polypeptide 0 (ICP0), which inhibits and terminates tumor necrosis factor (TNF)-α and Toll-like receptor (TLR)-mediated NF-κB activation (Daubeuf et al., 2009) and also degrades IFI16 to block DNA sensing (Lanfranca et al., 2014); these changes suppress the host-cell innate immunity and thereby promote viral infection. Here, NFKB1 is linked to viral infectious disease.