Biological Engineering Department, Southwest Guizhou Vocational and Technical College for Nationalitie, Xingyi, 562400, China; Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Key Laboratory of Veterinary Biological Engineering and Technology, Ministry of Agriculture, Nanjing, 210014, China.
College of Animal Science, Guizhou University, Guiyang, 550025, China; Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Key Laboratory of Veterinary Biological Engineering and Technology, Ministry of Agriculture, Nanjing, 210014, China.
Microb Pathog. 2022 Aug;169:105642. doi: 10.1016/j.micpath.2022.105642. Epub 2022 Jun 13.
Caprine parainfluenza virus type 3 (CPIV3), a new strain of virus, was isolated from the goats in 2014 in China. Studies have shown that viral infection can induce changes in the expression profile of host miRNAs, which modulate natural immune responses and viral infection. In this study, we report that bta-miR-677 suppressed CPIV3 replication in Madin-Darby bovine kidney (MDBK) cells and guinea pigs. Bta-miR-677 overexpression promoted type I interferon (IFN-I) and IFN-stimulated genes (ISGs) production, thereby inhibiting CPIV3 replication, while bta-miR-677 inhibitor suppressed the antiviral innate immune response to promoted viral replication in MDBK cells. We showed that bta-miR-677 suppresses CPIV3 replication via directly targeted the 3'-untranslated region (3'-UTR) of mitochondrial antiviral signaling protein (MAVS) thus enhancing IFN pathway in MDBK cells. We also demonstrated that bta-miR-677 agomir could inhibit CPIV3 proliferation in guinea pigs, with much lower viral RNA levels in lung and trachea. Guinea pigs showed no obvious pathological changes and less severe lung lesions in bta-miR-677 agomir treated group at 7 dpi. This study contributes to our understanding of the molecular mechanisms underlying CPIV3 pathogenesis.
羊副黏病毒 3 型（CPIV3）是一种新型病毒，于 2014 年在中国从山羊中分离得到。研究表明，病毒感染可诱导宿主 miRNA 表达谱发生变化，从而调节天然免疫反应和病毒感染。本研究报告称，bta-miR-677 可抑制 MDBK 细胞和豚鼠中的 CPIV3 复制。bta-miR-677 的过表达促进了 I 型干扰素（IFN-I）和 IFN 刺激基因（ISGs）的产生，从而抑制 CPIV3 的复制，而 bta-miR-677 抑制剂则抑制了抗病毒固有免疫反应，从而促进了 MDBK 细胞中的病毒复制。我们表明，bta-miR-677 通过直接靶向线粒体抗病毒信号蛋白（MAVS）的 3'-非翻译区（3'-UTR）抑制 CPIV3 复制，从而增强了 MDBK 细胞中的 IFN 途径。我们还证明，bta-miR-677 agomir 可抑制豚鼠中的 CPIV3 增殖，使肺部和气管中的病毒 RNA 水平显著降低。在 bta-miR-677 agomir 处理组中，豚鼠在 7dpi 时未显示明显的病理变化，肺部病变也较轻。本研究有助于我们了解 CPIV3 发病机制的分子机制。
