EV71抑制I型干扰素信号通路中ISGF3的核转位

目的探讨肠道病毒71型（enterovirus71，EV71）感染对I型干扰素信号通路中核转位复合物干扰素刺激基因因子3（ISGF3）核转位的影响。方法Western印迹检测VRl432感染VeroE6对干扰素诱导的sTATl和STAT2磷酸化的影响。将pEGFP-C1-STATl重组质粒转染VeroE6细胞，随后进行EV71感染以及IFN-ot2b刺激，将细胞进行亚细胞分离检测ISGF3的核转位情况。结果VRl432以感染复数（MOI）为1感染VeroE6细胞后未影响干扰素刺激的STATl和STAT2的磷酸化；亚细胞分离后Western印迹检测磷酸化的STATl，结果显示VRl432感染后，p-STATl在细胞核内表达水平明显降低，说明Ev71感染抑制了p-STATl的核转位。结论EV71感染抑制I型干扰素信号通路中ISGF3（STATl／STAT2／IRF9）的核转位，从而影响干扰素效应途径中抗病毒蛋白的表达。

EV71 inhibits nuclear translocation of ISGF3 in type I interferon signaling pathway

Objective To explore the effect of enterovirus 71 （EVT1） infection on the interferon-stimulated gene factor 3 （ISGF3） nuclear translocation in type I IFN signaling pathway. Methods The phosphorylation levels of STAT1 and STAT2 in Vero E6 cells were detected by Western blotting in the presence or absence of VR1432 infection after IFN-ct treatment. Vero E6 cells were transfected with pEGFP-C1-STAT1 and subsequently infected with VR1432 virus. The cells were treated with IFN-ot2b before harvest. Nuclear-cytosol extraction was conducted to examine the translocation of ISGF3 in EV71-infected cells. Results Western blotting showed that VR1432 infected at multiplicity of infection（MOI） of 1 did not alter the total IFN-induced phosphorylation of STAT1, but the phosphorylation of STAT1 was significantly reduced in the nuclei of VR1432-infected cells after IFN-a2b treatment. Conclusion VR1432 virus inhibits the nuclear translocation of IFN-induced ISGF3.