1College of Basic Medical Sciences, Jinzhou Medical University, Jinzhou 121200, Liaoning, PR China.
2Biological Anthropology institute, Jinzhou Medical University, Jinzhou 121200, Liaoning, PR China.
J Gen Virol. 2019 Apr;100(4):616-628. doi: 10.1099/jgv.0.001231. Epub 2019 Feb 6.
Human astrovirus non-structural protein nsP1a/4, located at the C-terminal end of nsP1a, is thought to be involved in regulating RNA replication. Here, we show that host protein CD63 interacts with the nsP1a protein. Further research showed that the large loop (LEL) domain of CD63 also interacts with nsP1a/4. Confocal microscopy showed that nsP1a/4 protein and CD63 co-localized in the cytoplasm of co-transfected cells. Co-localization of nsP1a/4 and CD63 was also observed in HAstV-1-infected cells. Overexpression of CD63 promoted replication of HAstV-1, whereas knockdown of CD63 reduced production of HAstV-1 viral progeny. These results suggest that CD63 plays a critical role in HAstV-1 replication, and provide an avenue to further understanding the interactions between host and virus proteins during replication and pathogenesis of HAstV.
人星状病毒非结构蛋白 nsP1a/4，位于 nsP1a 的 C 末端，被认为参与调节 RNA 复制。在这里，我们表明宿主蛋白 CD63 与 nsP1a 蛋白相互作用。进一步的研究表明，CD63 的大环（LEL）结构域也与 nsP1a/4 相互作用。共聚焦显微镜显示 nsP1a/4 蛋白和 CD63 在共转染细胞的细胞质中共定位。在 HAstV-1 感染的细胞中也观察到 nsP1a/4 和 CD63 的共定位。CD63 的过表达促进了 HAstV-1 的复制，而 CD63 的敲低则减少了 HAstV-1 病毒后代的产生。这些结果表明 CD63 在 HAstV-1 复制中起着关键作用，并为进一步了解 HAstV 复制和发病机制中宿主和病毒蛋白之间的相互作用提供了途径。
