Shen Xuehuai, Yin Lei, Pan Xiaocheng, Zhao Ruihong, Zhang Danjun
Institute of Animal Husbandry and Veterinary Science, Anhui Academy of Agricultural Sciences, Hefei, Anhui, 230031, China; Livestock and Poultry Epidemic Diseases Research Center of Anhui Province, Hefei, Anhui, 230031, China.
Institute of Animal Husbandry and Veterinary Science, Anhui Academy of Agricultural Sciences, Hefei, Anhui, 230031, China; Livestock and Poultry Epidemic Diseases Research Center of Anhui Province, Hefei, Anhui, 230031, China.
Microb Pathog. 2020 Oct;147:104378. doi: 10.1016/j.micpath.2020.104378. Epub 2020 Jul 10.
Porcine epidemic diarrhea virus (PEDV) is responsible for the acute infectious swine disease porcine epidemic diarrhea (PED). PED causes damage to the intestine, including villus atrophy and shedding, leading to serious economic losses to the pig industry worldwide. We carried out an in vitro study to investigate cell apoptosis and the cell cycle in a PEDV-infected host using transcriptomic shotgun sequencing (RNA-Seq) to study gene responses to PEDV infection. Results revealed that the PEDV infection reduced proliferation activity, blocked the cell cycle at S-phase and induced apoptosis in IPEC-J2 cells. The expression of gene levels related to ribosome proteins and oxidative phosphorylation were significantly up-regulated post-PEDV infection. Although the significantly down-regulated on PI3K/Akt signaling pathway post-PEDV infection, the regulator-related genes of mTOR signaling pathway exerted significantly up-regulated or down-regulated in IPEC-J2 cells. These results indicated that ribosome proteins and oxidative phosphorylation process were widely involved in the pathological changes and regulation of host cells caused by PEDV infection, and PI3K/AKT and mTOR signaling pathways played a vital role in antiviral regulation in IPEC-J2 cells. These data might provide new insights into the specific pathogenesis of PEDV infection and pave the way for the development of effective therapeutic strategies.
猪流行性腹泻病毒(PEDV)是引起猪急性传染病猪流行性腹泻(PED)的病原体。PED会对肠道造成损害,包括绒毛萎缩和脱落,给全球养猪业带来严重的经济损失。我们开展了一项体外研究,利用转录组鸟枪法测序(RNA-Seq)研究PEDV感染宿主中的细胞凋亡和细胞周期,以探究基因对PEDV感染的反应。结果显示,PEDV感染降低了增殖活性,使IPEC-J2细胞的细胞周期阻滞在S期,并诱导细胞凋亡。PEDV感染后,与核糖体蛋白和氧化磷酸化相关的基因水平表达显著上调。虽然PEDV感染后PI3K/Akt信号通路显著下调,但mTOR信号通路的调节相关基因在IPEC-J2细胞中表现出显著上调或下调。这些结果表明,核糖体蛋白和氧化磷酸化过程广泛参与了PEDV感染引起的宿主细胞病理变化和调控,PI3K/AKT和mTOR信号通路在IPEC-J2细胞的抗病毒调控中发挥了重要作用。这些数据可能为PEDV感染的具体发病机制提供新的见解,并为开发有效的治疗策略铺平道路。