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Caprine parainfluenza virus type 3 N protein promotes viral replication via inducing apoptosis

文献类型： 外文期刊

作者： Li, Jizong 1 ; Yang, Leilei 1 ; Mao, Li 1 ; Li, Wenliang 1 ; Sun, Min 1 ; Liu, Chuanmin 1 ; Xue, Tao 2 ; Zhang, Wenwen 1 ; L 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Vet Med, Key Lab Vet Diag, Key Lab Vet Biol Engn & Technol,Minist Agr, Nanjing 210014, Peoples R China

2.Linyi Univ, Sch Pharm, Linyi 276000, Shandong, Peoples R China

3.Jiangsu Univ, Sch Food & Biol Engn, Inst Life Sci, Zhenjiang 212013, Jiangsu, Peoples R China

4.Nanjing Agr Univ, Coll Vet Med, Nanjing 210095, Peoples R China

关键词： Caprine parainfluenza virus type 3; Goat tracheal epithelial cells; Apoptosis; N protein; Viral replication

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： 2021 年 259 卷

页码：

收录情况： SCI

摘要： Caprine parainfluenza virus type 3 (CPIV3) is one of the most important viral respiratory pathogens of goat. Accumulating evidence demonstrates that apoptosis is a cellular mechanism for the host response to pathogens, and it participates in regulating viral replication. However, there is little study on CPIV3-induced host cells apoptosis. In this study, primary goat tracheal epithelial (GTE) cells were established as a cellular model that is permissive to CPIV3 infection. Then, we showed that CPIV3 infection induced apoptosis in GTE cells, as determined by morphological changes, flow cytometry and TUNEL assay. Moreover, Caspase activity and the expression of pro-apoptotic genes further suggested that CPIV3 induced apoptosis by activating both the intrinsic and extrinsic pathways. Mechanistically, the ability of CPIV3 to induce apoptosis was activated by N protein, and the viral protein increased CPIV3 replication through effecting apoptosis. Overall, our findings showed that GTE cells that will enable further analysis of CPIV3 infection and offers novel insights into the mechanisms of CPIV3induced apoptosis in host cells.

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