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首页> 外文期刊>Journal of proteome research >Differential Protein Analysis of IPEC-J2 Cells Infected with Porcine Epidemic Diarrhea Virus Pandemic and Classical Strains Elucidates the Pathogenesis of Infection
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Differential Protein Analysis of IPEC-J2 Cells Infected with Porcine Epidemic Diarrhea Virus Pandemic and Classical Strains Elucidates the Pathogenesis of Infection

机译:用猪流行性腹泻病毒大流行病和古典菌感染的IPEC-J2细胞的差异蛋白质分析阐明了感染的发病机制

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Porcine epidemic diarrhea (PED) re-emerged in China in late 2010 and has now become widespread. Accumulated evidence indicates that this large-scale outbreak of diarrhea Was caused by variants of the highly virulent porcine epidemic diarrhea virus (PEDV). A pandemic PEDV YC2014 strain (YC2014) was isolated from clinical samples. 6 An iTRAQ-based comparative quantitative proteomic study of IPEC-J2 cells infected with YC2014 and a classical CV777 strain (CV777) was performed to determine the differences between pandemic and classical PEDV strain infection. Totals of 353 and 299 differentially expressed proteins were identified upon YC2014 and CV777 infection, respectively. The canonical pathways and functional networks involved in both PEDV infections were analyzed. The results indicated that the PEDV suppressed protein synthesis of IPEC-J2, cells through down-regulation of the PI3K-AKT/mTOR signaling pathways. Infection with YC2014 could activate the JAK-STAT signaling pathway and the NF-kappa B pathway more intensively than CV777. YC2014 could activate NF-kappa B pathway more intensively than CV777. On the basis of differentially expressed proteins, we propose that PEDV might disrupt apoptosis and may elicit stronger inflammatory cascades as well. This study might contribute to an understanding of the pathogenesis of PEDV infection and aid in the development of effective preventive and control vaccines.
机译:猪流行病腹泻(PED)在2010年底在中国重新出现,现已变得普遍。积累的证据表明,这种大规模的腹泻爆发是由高毒性猪流行病毒腹泻病毒(PEDV)的变异引起的。从临床样品中分离出大流行PEDV YC2014菌株(YC2014)。 [6进行了基于ITRAQ的对比定量蛋白质组学研究,对YC2014感染的IPEC-J2细胞和经典CV777菌株(CV777)以确定大流行和典型PEDV菌株感染的差异。在YC2014和CV777感染时鉴定了353和299型差异表达蛋白质的总数。分析了涉及PEDV感染的规范途径和功能网络。结果表明,PEDV抑制了IPEC-J2,细胞的蛋白质合成,通过对PI3K-AKT / MTOR信号传导途径的下调。用YC2014感染可以比CV777更强烈地激活Jak-Stat信号通路和NF-Kappa B路径。 YC2014可以比CV777更集中激活NF-Kappa B路径。在差异表达蛋白质的基础上,我们提出了PEDV可能会破​​坏细胞凋亡,也可能引起更强的炎症级联。该研究可能有助于了解PEDV感染的发病机制,并有助于开发有效预防和对照疫苗。

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