Fig. 1

HSV-1 mediated evasion of the type I IFN signal pathway. PRRs, such as TLRs, RLRs and cytosolic DNA sensors, could recognize pathogen-associated molecular patterns. TLRs locate both at the plasma membrane and endosomes, and signal through TRIF and MyD88 to lead the activation of IRFs and NF-κB. RIG-I and MDA5 detect distinct RNA structures and signal through the adaptor protein MAVS to trigger IRF3 and NF-κB activation. cGAS recognizes dsDNA in the cytosol and subsequently catalyzes the production of cGAMP, a second messenger that activates the ER-localized adaptor protein STING. STING recruits and activates TBK1, which then activates IRF3 to induce type I IFNs. Multiple steps in the type I IFN signal pathway can be hijacked by HSV-1 proteins. Green full lines indicate confirmed interactions between host molecules and HSV-1 proteins. Green dashed lines indicate uncertain interactions that need to be further studied