口蹄疫病毒（FMDV）感染机体后能够引起机体I型干扰素（IFN）下调从而抑制机体的先天性免疫应答，使得病毒在动物体内迅速复制。目前国内外对FMDV的L蛋白和3C蛋白抑制机体I型IFN的信号通路的机制做了研究，而对FMDV抑制II型IFN信号通路的机制未做任何研究报道。我们之前的研究已经通过Luciferase试验等证实3C蛋白能够抑制II型IFN信号通路。在此基础上，本项目将从JAK-STAT信号通路来研究3C蛋白抑制II型IFN信号通路的机制，并进一步筛选3C蛋白上抑制JAK-STAT信号通路的关键氨基酸功能位点，阐明FMDV 3C蛋白影响抑制II型IFN信号通路的分子机理，为预防和控制FMDV感染提供新的靶向分子。

Foot-and-mouth disease virus (FMDV) infection could down-regulate type I interferon (IFN) to suppress host innate immune response. It was reported that L protein and 3C protein of FMDV could down-regulate type I IFN, but there was no report about proteins of FMDV down-regulating type II IFN. We have already found that 3C protein could down-regulate the activity of IFN γ promoter using luciferase assay. The mechanisms of FMDV 3C protein down-regulating type II IFN would be further studied from JAK-STAT signaling pathway. In addition, the key amino acides of 3C protein which involved in inhibiting the JAK-STAT signaling pathway would be screened. Therefore, the project will systematically study and elucidate the mechanism of FMDV 3C protein antagonizing the type II IFN signaling pathway. It will provide new target molecules for the prevention and control of FMDV infection.