CD59 与传染性支气管炎病毒粒子的结合可防止抗体依赖性补体介导的溶解。
CD59 association with infectious bronchitis virus particles protects against antibody-dependent complement-mediated lysis.
机构信息
State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Xujiaping 1, Lanzhou, Gansu 730046, PR China.
Guangdong Province Key Laboratory Microbial Signals and Disease Co, and Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou, Guangdong 510642, PR China.
出版信息
J Gen Virol. 2017 Nov;98(11):2725-2730. doi: 10.1099/jgv.0.000962. Epub 2017 Oct 25.
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.
CD59 蛋白通过与 C8/C9 因子结合，作为补体系统末端途径的负调节剂发挥作用。迄今为止，人们对 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。在本研究中，我们发现 CD59 在 IBV 感染的细胞中下调，并与 IBV 病毒粒子相关。这种关联保护 IBV 颗粒免受抗体依赖性补体介导的裂解。当细胞中过表达 CD59 蛋白后再感染 IBV 时，上清液中的 IBV 滴度显著增加，而敲低或切割 CD59 进一步支持了这一观察结果。由于从过表达、敲低或切割 CD59 组制备的总细胞裂解物中未检测到 IBV N 蛋白和病毒 RNA 水平的明显变化，我们的数据表明 CD59 参与了 IBV 颗粒的释放，并且 IBV 已经进化出一种利用 CD59 逃避补体介导破坏的机制。
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