Porcine circovirus-like virus P1 activates pancreatic secretion pathway by interacting with CHRM3 protein

文献类型： 外文期刊

第一作者： Zhu, Jiaping

作者： Zhu, Jiaping;Yin, Lihong;Zhang, Fengxi;Suolang, Sizhu;Zhu, Jiaping;Xiao, Qi;Yin, Lihong;Zhang, Fengxi;Wen, Libin;He, Kongwang;Xiao, Qi;Wen, Libin;He, Kongwang;Xiao, Qi;Wen, Libin;He, Kongwang

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关键词： P1 virus; CHRM3; Pancreatic secretory pathway; PMWS; VP1 protein

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.246； 五年影响因子：3.565 ）

ISSN： 0378-1135

年卷期： 2022 年 272 卷

页码：

收录情况： SCI

摘要： The porcine circovirus-like virus P1, a member of the circovirus family, causes post-weaning multisystemic wasting syndrome (PMWS) in weaned piglets with progressive wasting as the main clinical symptom. The pancreatic secretion pathway induces pancreatic acinar cells to secrete various digestive enzymes and as such is an important signaling pathway for the digestive system and somatic growth. This study examined the effects and mechanism of P1 virus infection on the pancreatic secretion pathway. The experiment was conducted by transfecting double-copy plasmid P1 into PK-15 and 3D4 cells and by infecting cells with the P1 virus. Samples were collected at various times after transfection or infection. The pathway's transcription and translation levels of CHRM3, Gq, PLC-beta 2, PRKCA, Rab3D, RhoA, Rac1, and amyA proteins were detected by real-time PCR and Western blots; these analyses confirmed that the P1 virus infection could upregulate the expression level of key pancreatic secretion signaling molecules. Then, we confirmed that the VP1 protein of the P1 virus could interact with the pathway initiation protein CHRM3 using Co-IP, pull-downs, and confocal fluorescence microscopy. Finally, we demonstrated that the VP1 protein activates the pancreatic secretory pathway through the CHRM3 protein. In conclusion, this study demonstrated that the P1 virus can interact with the CHRM3 receptor protein to activate the pancreatic secretion pathway and promote the secretion of various digestive enzymes downstream of the pathway, thereby providing a basis for P1 virus pathogenesis.

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