MicroRNA miR-214 inhibits snakehead vesiculovirus replication by targeting the coding regions of viral N and P.
MicroRNA miR-214 inhibits snakehead vesiculovirus replication by targeting the coding regions of viral N and P.
复制标题
MicroRNA miR-214 通过靶向病毒 N 和 P 编码区抑制蛇头水泡病毒复制
DOI：
10.1099/jgv.0.000854
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发表时间：
2017
影响因子：
3.8
通讯作者：
Tu Jiagang
中科院分区：
文献类型：
--
作者：
Zhang Chi;Yi Lizhu;Feng Shuangshuang;Liu Xueqin;Su Jianguo;Lin Li;Tu Jiagang
蛇头水泡病毒是弹状病毒科的一个新成员，近年来在中国的蛇头养殖业中造成了巨大的经济损失，但对其致病的分子机制却知之甚少。MicroRNAs(MiRNAs)是一种在病毒感染中发挥重要作用的非编码小RNA。在这项研究中，我们发现SHVV感染以时间和剂量依赖的方式下调条纹蛇头(SSN-1)细胞miR-214的表达。值得注意的是，用miR-214转染SSN-1细胞模拟显著抑制SHVV复制，而miR-214抑制SHVV复制，提示miR-214对SHVV复制起负调控作用。我们的研究进一步证明SHVV的N和P是miR-214的靶基因。在SHVV感染的细胞中，过表达P而不是N抑制了干扰素-α的产生，这种抑制可以通过过表达miR-214来恢复。综上所述，这些结果表明，在SHVV感染过程中miR-214表达下调，miR-214下调反过来又增加了N和P的表达，减少了干扰素-α的产生，从而促进了SHVV的复制。本研究为更好地了解SHVV致病的分子机制和抗SHVV感染的潜在策略提供了依据。
Snakehead vesiculovirus (SHVV), a new member of the family Rhabdoviridae, has caused enormous economic losses in.snakehead fish culture during the past years in China; however, little is known about the molecular mechanisms of its.pathogenicity. MicroRNAs (miRNAs) are small non-coding RNAs that play important roles in virus infection. In this study, we.identified that SHVV infection downregulated miR-214 in striped snakehead (SSN-1) cells in a time- and dose-dependent.manner. Notably, transfecting SSN-1 cells with miR-214 mimic significantly inhibitedSHVV replication, whereas miR-214.inhibitor promoted it, suggesting that miR-214 acted as a negative regulator of SHVV replication. Our study further.demonstrated that N and P of SHVV were the target genes of miR-214. Over-expression of P, but not N, inhibited IFN-a.production in SHVV-infected cells, which could be restored by over-expression of miR-214. Taken together, these results.suggest that miR-214 is downregulated during SHVV infection, and the downregulated miR-214 in turn increased N and P.expression and decreased IFN-a production, thus facilitating SHVV replication. This study provides a better understanding of.the molecular mechanisms on the pathogenesis of SHVV and a potential antiviral strategy against SHVV infection.