CD59 association with infectious bronchitis virus particles protects against antibody-dependent complement-mediated lysis
CD59 association with infectious bronchitis virus particles protects against antibody-dependent complement-mediated lysis
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CD59 与传染性支气管炎病毒颗粒的关联可防止抗体依赖性补体介导的裂解
DOI：
10.1099/jgv.0.000962
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发表时间：
2017
影响因子：
3.8
通讯作者：
Sun Shiqi
中科院分区：
文献类型：
--
作者：
Wei Yanquan;Ji Yanhong;Guo Huichen;Zhi Xiaoying;Han Shichong;Zhang Yun;Gao Yuan;Yan Dan;Li Kangyu;Liu Ding Xiang;Sun Shiqi
CD59蛋白通过与C8/C9因子结合而作为补体系统末端途径的负调节剂发挥作用。迄今为止，对CD59在冠状病毒传染性支气管炎病毒（IBV）感染中的作用知之甚少。在这项研究中，我们发现CD59在IBV感染的细胞中下调，并与IBV病毒粒子相关。这种结合保护IBV颗粒免受抗体依赖性补体介导的裂解。当CD59蛋白在细胞中过表达，随后IBV感染时，上清液中的IBV滴度显著增加，并且该观察结果进一步得到CD59敲低或切割的支持。由于在从CD59组的过表达、敲低或裂解制备的总细胞裂解物中未检测到IBV N蛋白和病毒RNA水平的显著变化，我们的数据表明CD59参与IBV颗粒释放，并且IBV已经进化出利用CD59逃避补体介导的破坏的机制。
CD59 protein functions as a negative regulator of the terminal pathway of the complement system by binding to the C8/C9 factors. To date, little is known about the role of CD59 in coronavirus infectious bronchitis virus (IBV) infection. In this study, we discovered that CD59 was downregulated in IBV-infected cells and was associated with IBV virions. This association protected IBV particles from antibody-dependent complement-mediated lysis. IBV titres in the supernatant were significantly increased when CD59 proteins were overexpressed in cells followed by IBV infection, and this observation was further supported by knockdown or cleavage of CD59. Because no considerable change in IBV N protein and viral RNA levels was detected in total cell lysates prepared from the overexpression, knockdown or cleavage of CD59 groups, our data indicated that CD59 was involved in IBV particle release and that IBV had evolved a mechanism to utilize CD59 to evade complement-mediated destruction.