野鸭源新城疫病毒V蛋白抑制宿主细胞干扰素β产生的机制研究  

Mechanism of V protein of mallard Newcastle disease virus inhibiting production of IFN-β of host cells

作　　者：田志革[1,2] 黄峰华[1] 华育平[2] 

机构地区：[1]黑龙江省农业科学院信息中心,黑龙江哈尔滨150086 [2]东北林业大学野生动物资源学院,黑龙江哈尔滨150040

出　　处：《中国兽医科学》2016年第7期874-878,共5页Chinese Veterinary Science

基　　金：中央高校基本科研业务费专项资金项目(2572014AA03);林业公益性行业科研专项(20140404)

摘　　要：为研究野鸭源新城疫病毒(ND V)V蛋白抑制宿主细胞干扰素β(IFN-β)产生的机制,构建真核表达新城疫病毒强、弱毒株V蛋白的重组载体,分别与IFN-β-Luc、NF-κB-Luc、PRDⅢ/Ⅰ-Luc、AP-1-Luc报告质粒共转染H EK-293T细胞,接种仙台病毒刺激宿主细胞后,测定宿主细胞的相对荧光素酶活性。结果显示,新城疫病毒强毒株V蛋白(vNDV-V)能抑制NF-κB、AP-1、PRDⅢ/Ⅰ启动子活性,新城疫病毒弱毒株V蛋白(aNDV-V)能抑制NF-κB、AP-1启动子活性,进而抑制IFN-β的产生。构建新城疫强弱病毒V蛋白嵌合体进行试验,结果表明NDV强毒株V蛋白羧基端在抑制PRDⅢ/Ⅰ启动子活性中发挥关键作用。研究结果为深入研究V蛋白对抗宿主细胞天然免疫机制奠定了基础。The aim of the study was to research the mechanism of V protein of mallard Newcastle disease virus（NDV） inhibiting production of IFN-β of host cells. The recombinant plasmids expressing V proteins of virulent（vNDV-V） and avirulent NDV（aNDV-V） were constructed. The HEK-293T cells were cotransfected with the recombinant plasmids and report gene plasmids IFN-β-Luc,NF-KB-Luc,PRD Ⅲ/Ⅰ-Luc and AP-1-Luc respectively. After the cells were stimulated by Sendai virus,the relative luciferase activity was determined. The results showed that the vNDV-V markedly inhibited IFN-β-production by decreasing NF-KB, AP-1,PRDⅢ/Ⅰ activities and the aNDV-V inhibited IFN-β-production by decreasing NF-κB and AP-1 activities. The C-terminal of vNDV-V had an important effect on the inhibition of PRDⅢ/Ⅰ activity. The results laid the foundation for further studying the mechanism of inhibiting innate immunity of host cells by V protein.

关 键 词：新城疫病毒 V蛋白 抑制 干扰素Β 

分 类 号：S852.659.5[农业科学—基础兽医学]