State Key Laboratory for Molecular Biology of Special Economic Animals, Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun, 130112, China.
Sci Rep. 2016 Jul 13;6:29560. doi: 10.1038/srep29560.
Canine parvovirus (CPV) reproduces by co-opting the resources of host cells, inevitably causing cytotoxic effects to the host cells. Feline kidney F81 cells are sensitive to CPV infection and show disparate growing statuses at different time points post-infection. This study analysed the response of F81 cells to CPV infection at successive infection time points by iTRAQ-based quantitative proteomics. Differentially expressed proteins (DEPs) during 60 h of infection and at selected time points post-infection were identified by an analysis of variance test and a two-tailed unpaired t test, respectively. DEPs with similar quantitative changes were clustered by hierarchical clustering and analysed by gene ontology enrichment, revealing that 12 h and 60 h post-infection were the optimal times to analyse the autonomous parvovirus replication and apoptosis processes, respectively. Using the Metacore(TM) database, 29 DEPs were enriched in a network involved in p53 regulation. Besides, a significantly enriched pathway suggests that the CPV-induced cytopathic effect was probably due to the deficiency of functional CFTR caused by CPV infection. This study uncovered the systemic changes in key cellular factors involved in CPV infection and help to understand the molecular mechanisms of the anti-cancer activity of CPV and the cytopathic effects induced by CPV infection.
犬细小病毒（CPV）通过利用宿主细胞的资源进行复制，不可避免地对宿主细胞造成细胞毒性作用。猫肾细胞 F81 对 CPV 感染敏感，在感染后不同时间点呈现出不同的生长状态。本研究通过 iTRAQ 定量蛋白质组学分析，在连续感染时间点分析了 F81 细胞对 CPV 感染的反应。通过方差分析和双尾非配对 t 检验分别鉴定了 60 h 感染期间和感染后选定时间点的差异表达蛋白（DEPs）。通过层次聚类对具有相似定量变化的 DEPs 进行聚类，并通过基因本体富集分析进行分析，结果表明 12 h 和 60 h 是分析自主细小病毒复制和凋亡过程的最佳时间。使用 Metacore（TM）数据库，在涉及 p53 调节的网络中富集了 29 个 DEP。此外，一个显著富集的途径表明，CPV 诱导的细胞病变效应可能是由于 CPV 感染导致 CFTR 功能缺失。本研究揭示了 CPV 感染中涉及的关键细胞因子的系统变化，有助于理解 CPV 抗癌活性和 CPV 感染诱导的细胞病变效应的分子机制。
