Interferon-stimulated genes inhibit caprine parainfluenza virus type 3 replication in Madin-Darby bovine kidney cells
文献类型： 外文期刊
作者： Li, Jizong 1 ; Mao, Li 1 ; Xiao, Fang 1 ; Liao, Zheng 1 ; Yin, Junlei 5 ; Li, Wenliang 1 ; Sun, Min 1 ; Liu, Maojun 1 ; Ji, 1 ;
作者机构： 1.Jiangsu Acad Agr Sci, Key Lab Vet Biol Engn & Technol, Minist Agr, Inst Vet Med,Key Lab Vet Diag, Nanjing 210014, Peoples R China
2.Linyi Univ, Sch Pharm, Linyi 276000, Shandong, Peoples R China
3.Jiangsu Univ, Sch Food & Biol Engn, Zhenjiang 212013, Jiangsu, Peoples R China
4.Guizhou Univ, Coll Anim Sci, Guiyang 550025, Peoples R China
5.Xinxiang Univ, Sch Life Sci & Technol, Xinxiang 453003, Henan, Peoples R China
关键词： Caprine parainfluenza virus type 3; MDBK cells; ISGs; RNA-Seq
期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）
ISSN： 0378-1135
年卷期： 2020 年 241 卷
页码：
收录情况： SCI
摘要： Caprine parainfluenza virus type 3 (CPIV3) is the one of most common causative agents of caprine respiratory infection, resulting in significant economic losses in the goat and sheep industries. However, the molecular mechanisms and host genes involved in the pathogenesis of and immunity against CPIV3 infection remain poorly understood. In this study, we used RNA-Seq to understand the responses of madin-darby bovine kidney (MDBK) cells to CPIV3 infection. A total of 261 differentially-expressed genes (DEGs) were identified in CPIV3-infected compared with mock-infected MDBK cells at 24 h post-infection (hpi). The DEGs were mainly involved in immune system processes, metabolic processes, and signal transduction. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis demonstrated that the most significantly enriched signaling pathways were MAPK, Wnt, PI3K-Akt, tumor necrosis factor, Toll-like receptor and ubiquitin-mediated proteolysis. STRING analysis revealed that seven interferon-stimulated genes (ISGs) were upregulated (IFI6, ISG15, OAS1Y, OASIZ, MX1, MX2 and RSAD2) and may play a pivotal role during CPIV3 infection. Moreover, overexpression of these ISGs significantly reduced CPIV3 replication in vitro, while siRNA silencing markedly improved CPIV3 replication 24 and 48 hpi. Ours is the first study to profile the gene expression of CPIV3-infected MDBK cells. We identified seven ISGs that could be targeted in novel antiviral strategies against CPIV3.
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