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Interferon (IFN)-mediated innate immune defense is a potent antiviral mechanism.Viruses evade innate immunity and limit secretion of IFN-β to replicate and survive in the host.The largest tegument protein of herpes simplex virus 1 (HSV-1), UL36, contains a novel deubiquitinase (DUB) motif embedded in its N-terminus, denoted as UL36 ubiquitin-specific protease (UL36USP).In the present study, we demonstrated that HSV-1 UL36USP inhibited the Sendai virus (SeV) induced IRF3 dimerization, promoter activation and transcription of IFN-β.