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首页> 外文期刊>Journal of proteomics >Cellular proteome alterations in response to enterovirus 71 and coxsackievirus A16 infections in neuronal and intestinal cell lines
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Cellular proteome alterations in response to enterovirus 71 and coxsackievirus A16 infections in neuronal and intestinal cell lines

机译:响应肠道病毒71和柯萨奇病毒A16感染的神经元和肠细胞系细胞蛋白质组改变

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摘要

Hand, foot and mouth disease is mainly caused by enterovirus A71 (EV-A71) and coxsackievirus A16 (CV-A16), but EV-A71 is also associated with severe neurological complications. Host factors may contribute to the different clinical outcomes of EV-A71 and CV-A16 infections. A neurovirulent EV-A71 strain (EV-A71/UH1) from a fatal case, a non-neurovirulent EV-A71 strain (EV-A71/Sha66) and a CV-A16 strain (CV-A16/22159) from cases of uncomplicated HFMD were used. Replication of the viruses in SK-N-MC (neuronal) and HT-29 (intestinal) cell lines correlated with the severity of clinical disease associated with each virus. EV-A71/UH1 showed the greatest replication in neuronal cells. In HT-29 cells, both EV-A71 strains replicated well, but CV-A16/22159 showed no effective replication. The proteomes of mock and infected SK-N-MC and HT-29 cell lines were compared by 2D-SDS-PAGE. The differentially expressed proteins were identified by MALDI-TOF/TOF analysis. There were 46 and 44 differentially expressed proteins identified from SK-N-MC and HT-29 cells, respectively, categorized under apoptosis, stress, cytoskeletal, energy metabolism proteins and others. Western blot validation showed that EV-A71/UH1 and CV-A16 also differentially induced proteins involved in viral RNA translation and host cell stress responses in neuronal and intestinal cell lines. (C) 2015 Elsevier B.V. All rights reserved.
机译:手足口病主要由肠道病毒A71(EV-A71)和柯萨奇病毒A16(CV-A16)引起,但EV-A71也与严重的神经系统并发症有关。宿主因素可能导致EV-A71和CV-A16感染的不同临床结果。致命病例的神经毒性EV-A71株(EV-A71 / UH1),非复杂病例的非神经毒性EV-A71株(EV-A71 / Sha66)和CV-A16株(CV-A16 / 22159)使用手足口病。病毒在SK-N-MC(神经元)和HT-29(肠)细胞系中的复制与每种病毒相关的临床疾病的严重程度有关。 EV-A71 / UH1在神经元细胞中显示出最大的复制。在HT-29细胞中,两种EV-A71菌株均复制良好,但CV-A16 / 22159未显示有效复制。通过2D-SDS-PAGE比较模拟和感染的SK-N-MC和HT-29细胞系的蛋白质组。通过MALDI-TOF / TOF分析鉴定了差异表达的蛋白质。从SK-N-MC和HT-29细胞中分别鉴定出46种和44种差异表达的蛋白质,分别归类于细胞凋亡,应激,细胞骨架,能量代谢蛋白质等。蛋白质印迹验证表明,EV-A71 / UH1和CV-A16也差异诱导了蛋白质,参与神经细胞和肠道细胞系中病毒RNA的翻译和宿主细胞的应激反应。 (C)2015 Elsevier B.V.保留所有权利。

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