It is well known that the early activation of NF-κB may promote the efficient replication of the virus (48), and thus, HSV-1 takes advantage of UL31 to activate NF-κB for initiating viral gene transcription in the early stage of viral infection, while HSV-1 again exploits UL31 to inhibit IFN-β for suppressing the host immune response and facilitating virus proliferation in the late stage of viral infection. The gene discussed is IFNB1; the disease is viral infectious disease.