FKBP8 interact with classical swine fever virus NS5A protein and promote virus RNA replication
FKBP8 interact with classical swine fever virus NS5A protein and promote virus RNA replication
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FKBP8与猪瘟病毒NS5A蛋白相互作用并促进病毒RNA复制
DOI：
10.1007/s11262-015-1286-6
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发表时间：
2016-02-01
期刊：
影响因子：
1.6
通讯作者：
Zhang, Yanming
中科院分区：
文献类型：
--
作者：
Li, Helin;Zhang, Chengcheng;Zhang, Yanming
猪瘟病毒(CSFV)的非结构5A(NS5A)蛋白被证明参与病毒复制，并通过其与多种细胞蛋白的相互作用来调节细胞信号和宿主细胞反应。据报道，FKBP8还可以促进病毒复制。在这里，我们通过免疫共沉淀和GST-Pull研究表明NS5A与FKBP8特异性相互作用。共聚焦显微镜观察发现，NS5A和FKBP8共定位于细胞质中。真核表达载体pDsRED N1过表达FKBP8可显著促进病毒RNA合成。慢病毒介导的shRNA对FKBP8细胞的敲除可显著降低CSFV感染后的病毒复制。这些数据表明，FKBP8在病毒生命周期中发挥着关键作用，特别是在病毒RNA复制期间。对FKBP8蛋白功能的研究可能有助于开发新的治疗CSFV感染的策略。
The non-structural 5A (NS5A) protein of classical swine fever virus (CSFV) is proven to be involved in viral replication and can also modulate cellular signaling and host cellular responses via to its ability to interact with various cellular proteins. FKBP8 is also reported to promote virus replication. Here, we show that NS5A specifically interacts with FKBP8 through coimmunoprecipitation and GST-pulldown studies. Additionally, confocal microscopy study showed that NS5A and FKBP8 colocalized in the cytoplasm. Overexpression of FKBP8 via the eukaryotic expression plasmid pDsRED N1 significantly promoted viral RNA synthesis. The cells knockdown of FKBP8 by lentivirus-mediated shRNA markedly decreased the virus replication when infected with CSFV. These data suggest that FKBP8 plays a critical role in the viral life cycle, particularly during the virus RNA replication period. The investigation of FKBP8 protein functions may be beneficial for developing new strategies to treat CSFV infection.