›› 2015, Vol. 42 ›› Issue (4): 1028-1031.doi: 10.16431/j.cnki.1671-7236.2015.04.039

• 疾病防治 • 上一篇    下一篇

口蹄疫病毒前导蛋白酶抑制宿主先天性免疫应答的机制

李夏莹1, 许文涛2,3, 汪其怀1   

  1. 1. 农业部科技发展中心, 北京 100122;
    2. 中国农业大学食品科学与营养工程学院, 北京 100083;
    3. 农业部转基因生物食用安全监督检验测试中心(北京), 北京 100083
  • 收稿日期:2014-10-31 出版日期:2015-04-20 发布日期:2015-05-05
  • 通讯作者: 汪其怀 E-mail:esmacloed006@163.com
  • 作者简介:李夏莹(1986-),女,云南玉溪人,博士,从事口蹄疫病毒蛋白与宿主细胞相互作用机制方面的研究,E-mail:esmacloed006@163.com
  • 基金资助:
    转基因生物新品种培育重大专项(2014ZX0801103B);食品质量与安全北京实验室

Mechanism of Foot-and-mouth Disease Virus Leader Protease to Inhibit Host Innate Immune Response

LI Xia-ying1, XU Wen-tao2,3, WANG Qi-huai1   

  1. 1. Development Center of Science and Technology, Ministry of Agriculture, Beijing 100122, China;
    2. College of Food Science and Nutrition Engineering, China Agricultural University, Beijing 100083, China;
    3. Supervision, Inspection & Testing Center of Genetically Modified Food Safety, Ministry of Agriculture, Beijing 100083, China
  • Received:2014-10-31 Online:2015-04-20 Published:2015-05-05

摘要: 口蹄疫是由口蹄疫病毒(foot-and-mouth disease virus,FMDV)引起的一种急性、热性、高度接触传染性动物疫病.口蹄疫病毒有多种机制对抗宿主的先天性免疫应答,在这个过程中病毒的前导蛋白酶(Lpro)发挥了关键作用.Lpro可切断宿主细胞帽子依赖性的蛋白翻译,抑制干扰素蛋白的合成;Lpro通过破坏核转录因子-κB (NF-κB)的完整性或减少干扰素调节因子3/7(IRF3/7)的表达,从而抑制IFN mRNA的产生;Lpro还会参与维甲酸诱导基因Ⅰ(RIG-Ⅰ)、TANK结合激酶1(TBK1)、TNF受体相关因子3(TRAF3)和TRAF6的去泛素化,从而影响Ⅰ型干扰素信号通路的活化.

关键词: 口蹄疫病毒; 前导蛋白酶; Ⅰ型干扰素; 先天性免疫应答

Abstract: Foot-and-mouth disease (FMD) is an acute, febrile, highly contagious animal disease caused by foot-and-mouth disease virus (FMDV). FMDV has a variety of mechanisms resisting host innate immune response, leader protease (Lpro) has played a key role in the process. Lpro can cut off the host cell cap-dependent translation, inhibiting the synthesis of interferon. Lpro through destroying the integrity of NF-κB or reducing the expression of IRF3/7, inhibits the production of interferons mRNA. Besides, Lpro can take part in the deubiquitination of reninoic-acid-inducible gene Ⅰ (RIG-Ⅰ), TANK binding kinase 1 (TBK1), TNF receptor-associate factor 3 (TRAF3) and TRAF6, thus affecting the activation of type Ⅰ interferon signaling pathway.

Key words: FMDV; leader protease; typeⅠinterferon; innate immune response

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