PI3K/AKT/p53 pathway inhibits infectious spleen and kidney necrosis virus infection by regulating autophagy and immune responses
文献类型： 外文期刊
作者： Zhang, Xiaoting 1 ; Ming, Yue 1 ; Fu, Xiaozhe 1 ; Niu, Yinjie 1 ; Lin, Qiang 1 ; Liang, Hongru 1 ; Luo, Xia 1 ; Liu, Lihui 1 ; Li, Ningqiu 1 ;
作者机构： 1.Chinese Acad Fishery Sci, Guangdong Prov Key Lab Aquat Anim Immune Technol, Minist Agr & Rural Affairs, Key Lab Fishery Drug Dev,Pearl River Fishery Res, Guangzhou 510380, Peoples R China
关键词： ISKNV; PI3K; AKT; p53; Autophagy; Antiviral target; Siniperca chuatsi
期刊名称：FISH & SHELLFISH IMMUNOLOGY （ 影响因子：4.622； 五年影响因子：4.799 ）
ISSN： 1050-4648
年卷期： 2022 年 120 卷
页码：
收录情况： SCI
摘要： The PI3K/AKT/p53 signaling pathway is activated by various types of cellular stimuli or pathogenic infection, and then regulates fundamental cellular functions to combat these stimulations. Here, we studied the meaningful roles of PI3K/AKT/p53 in regulating cellular machine such as autophagy, immune responses, as well as antiviral activity in Chinese perch brain (CPB) cells infected by infectious spleen and kidney necrosis virus (ISKNV), which is an agent caused devastating losses in mandarin fish (Siniperca chuatsi) industry. We found that ISKNV infection induced up-regulation of host PI3K/AKT/p53 axis, but inhibited autophagy in CPB cells. Interestingly, activation of PI3K/AKT/p53 axis factors trough agonists or overexpression dramatically decreased host autophagy level, inhibited ISKNV replication, and elevated the expression of immune-related genes in CPB cells. In contrast, suppression of PI3K/AKT/p53 pathway by inhibitors or small interfering RNA (siRNA)-mediated gene silence increased the autophagy and ISKNV replication, but down-regulated immune responses in CPB cells. All these results indicate that PI3K/AKT/p53 pathway plays an important role in anti-ISKNV infection and can be used as a new target for controlling ISKNV disease.
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