Porcine reproductive and respiratory syndrome virus infection induces microRNA novel-216 production to facilitate viral-replication by targeting MAVS 3<acute accent>UTR

作者全名：Luo, Xuegang; Xie, Sha; Xu, Xingsheng; Zhang, Yao; Huang, Yun; Tan, Dongmei; Tan, Yi

作者地址：[Luo, Xuegang] Chongqing Hlth Ctr Women & Children, Dept Obstet & Gynecol, 120 Longshan Rd, Chongqing 401147, Peoples R China; [Luo, Xuegang; Zhang, Yao; Huang, Yun; Tan, Dongmei; Tan, Yi] Chongqing Med Univ, Lab Anim Ctr, Yixueyuan Rd 1, Chongqing 400016, Peoples R China; [Luo, Xuegang] Chongqing Med Univ, Women & Childrens Hosp, Dept Obstet & Gynecol, 120 Longshan Rd, Chongqing 401147, Peoples R China; [Xie, Sha] Henan Univ Chinese Med, Zhengzhou 450002, Henan, Peoples R China; [Xu, Xingsheng] Southwest Univ, Coll Vet Med, Chongqing 402460, Peoples R China

通信作者：Tan, DM; Tan, Y (通讯作者)，Chongqing Med Univ, Lab Anim Ctr, Yixueyuan Rd 1, Chongqing 400016, Peoples R China.

来源：VETERINARY MICROBIOLOGY

ESI学科分类：PLANT & ANIMAL SCIENCE

WOS号：WOS:001224436500001

JCR分区：Q1

影响因子：2.4

年份：2024

卷号：292

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：PRRSV; miRNA; p38 signaling pathway; MAVS; IFN

摘要：Porcine reproductive and respiratory syndrome virus (PRRSV) has caused significant economic losses in the swine industry. In this study, the high-throughput sequencing, microRNAs (miRNAs) mimic, and lentivirus were used to screen for potential miRNAs that can promote PRRSV infection in porcine alveolar macrophages or Marc145 cells. It was observed that novel -216, a previously unidentified miRNA, was upregulated through the p38 signaling pathway during PRRSV infection, and its overexpression significantly increased PRRSV replication. Further analysis revealed that novel -216 regulated PRRSV replication by directly targeting mitochondrial antiviral signaling protein (MAVS), an upstream molecule of type I IFN that mediates the production and response of type I IFN. The proviral function of novel -216 on PRRSV replication was abolished by MAVS overexpression, and this effect was reversed by the 3 ' UTR of MAVS, which served as the target site of novel -216. In conclusion, this study demonstrated that PRRSV-induced upregulation of novel -216 served to inhibit the production and response of typeI IFN and facilitate viral replication, providing new insights into viral immune evasion and persistent infection.

基金机构：National Natural Science Foundation of China [32002294]; Chongqing Health Center for Women and Children; Chongqing Medical University

基金资助正文：<STRONG> </STRONG>This work was supported by the National Natural Science Foundation of China (Grant No.32002294) , Chongqing Health Center for Women and Children and the Chongqing Medical University