miR-124 attenuates Japanese encephalitis virus replication by targeting DNM2.
miR-124 attenuates Japanese encephalitis virus replication by targeting DNM2.
复制标题
miR-124通过靶向DNM2减弱日本脑炎病毒复制
DOI：
10.1186/s12985-016-0562-y
复制
发表时间：
2016-06-21
期刊：
影响因子：
4.8
通讯作者：
Zhao A
中科院分区：
文献类型：
--
作者：
Yang S;Pei Y;Li X;Zhao S;Zhu M;Zhao A
研究背景日本脑炎病毒（Japanese encephalitis virus，JEV）是一种由蚊媒传播的黄病毒，可引起人类急性病毒性脑炎。猪是乙脑病毒的重要放大宿主。越来越多的证据表明，宿主microRNAs（miRNAs）在调节病毒感染和发病机制中起着关键作用。然而，机制的研究描绘的作用，在调节主机JEV interactions仍然scarved.ResultsIn这项研究中，我们证明，miR-124抑制JEV复制在猪肾上皮PK 15细胞。此外，使用生物信息学工具，我们确定了dynamin 2（DNM 2），一个负责囊泡断裂的GT3，作为miR-124的靶点。小干扰RNA（siRNA）耗竭研究表明，dynamin 2是有效的JEV复制所必需的。我们还证明，在JEV感染的PK 15细胞中，miR-124的表达上调与其靶基因DNM 2的表达降低相对应。
BackgroundJapanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes acute viral encephalitis in humans. Pigs are important amplifier hosts of JEV. Emerging evidence indicates that host microRNAs (miRNAs) play key roles in modulating viral infection and pathogenesis. However, mechanistic studies delineating the roles of miRNAs in regulating host-JEV interactions remain scarce.ResultsIn this study, we demonstrated that miR-124 inhibited JEV replication in porcine kidney epithelial PK15 cells. Furthermore, using bioinformatics tools, we identified dynamin2 (DNM2), a GTPase responsible for vesicle scission, as a target of miR-124. Small interfering RNA (siRNA) depletion studies inicated that dynamin2 was required for efficient JEV replication. We also demonstrated that upregulation of miR-124 expression corresponded to decreased expression of its target, DNM2, in the JEV-infected PK15 cells.ConclusionsOverall, these results suggest the importance of miR-124 in modulating JEV replication and provide a scientific basis for using cellular miRNAs in anti-JEV therapies.