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Bta-miR-677 contribute to interferon pathway affecting the proliferation of caprine parainfluenza virus type 3

文献类型： 外文期刊

作者： Zhong, Chunyan 1 ; Liao, Zheng 2 ; Zhang, Baotai 2 ; Xiao, Li 2 ; Li, Jizong 3 ; Zhu, Xing 2 ;

作者机构： 1.Southwest Guizhou Vocat & Tech Coll Nationalitie, Biol Engn Dept, Xingyi 562400, Peoples R China

2.Guizhou Univ, Coll Anim Sci, Guiyang 550025, Peoples R China

3.Jiangsu Acad Agr Sci, Inst Vet Med, Minist Agr, Key Lab Vet Biol Engn & Technol, Nanjing 210014, Peoples R China

关键词： Caprine parainfluenza virus type 3; Bta-miR-677; Mitochondrial antiviral signaling protein; Interferon; IFN-Stimulated genes

期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.848； 五年影响因子：3.957 ）

ISSN： 0882-4010

年卷期： 2022 年 169 卷

页码：

收录情况： SCI

摘要： 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 & PRIME;- untranslated region (3 & PRIME;-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.

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