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鲤春病毒血症病毒的复制可受活性氧和NF-κB信号通路调控。

The replication of spring viraemia of carp virus can be regulated by reactive oxygen species and NF-κB pathway.

作者信息

Liu Lei, Tu Xiao, Shen Yu-Feng, Chen Wei-Chao, Zhu Bin, Wang Gao-Xue

机构信息

College of Animal Science and Technology, Northwest A&F University, Xinong Road 22nd, Yangling, Shaanxi 712100, China.

College of Animal Science and Technology, Northwest A&F University, Xinong Road 22nd, Yangling, Shaanxi 712100, China.

出版信息

Fish Shellfish Immunol. 2017 Aug;67:211-217. doi: 10.1016/j.fsi.2017.05.068. Epub 2017 Jun 8.

DOI:10.1016/j.fsi.2017.05.068
PMID:28602749
Abstract

Different viruses could induced ROS generation to alter intracellular redox state in the host cells, and unbalanced redox state was suggested to have various effects on viral replication. In this study, we investigated the influence of reactive oxygen species (ROS) on replication of spring viraemia of carp virus (SVCV) in fish cells. After SVCV infection, there existed a time-dependent increase in ROS generation. The present results revealed that antioxidant N-acetyl-l-cysteine (NAC) resulted in a lower ROS levels and increased SVCV replication in EPC cell. In contrast, a GSH synthesis inhibitor buthionine sulfoximine (BSO) induced ROS generation and decreased SVCV replication. In addition, activation of NF-κB suppressed SVCV replication by using two inhibitors of cytokine-induced IκBα phosphorylation. More importantly, enhancement of the activity of NF-κB was found in BSO treatment, which indicated that dropped SVCV replication likely occurred via ROS activation of NF-κB. Overall, our results revealed that the SVCV infection and replication could generate ROS and be affected by the redox state, where this progression was associated with the alteration in NF-κB pathway induced by oxidative stress.

摘要

不同病毒可诱导活性氧(ROS)生成,从而改变宿主细胞内的氧化还原状态,并且氧化还原状态失衡被认为对病毒复制有多种影响。在本研究中,我们调查了活性氧对鲤鱼春季病毒血症病毒(SVCV)在鱼类细胞中复制的影响。SVCV感染后,ROS生成呈时间依赖性增加。目前的结果显示,抗氧化剂N-乙酰-L-半胱氨酸(NAC)可降低ROS水平,并增加EPC细胞中SVCV的复制。相反,谷胱甘肽合成抑制剂丁硫氨酸亚砜胺(BSO)诱导ROS生成并减少SVCV复制。此外,通过使用两种细胞因子诱导的IκBα磷酸化抑制剂激活NF-κB可抑制SVCV复制。更重要的是,在BSO处理中发现NF-κB活性增强,这表明SVCV复制下降可能是通过ROS激活NF-κB发生的。总体而言,我们的结果显示,SVCV感染和复制可产生活性氧并受氧化还原状态影响,其中这一进程与氧化应激诱导的NF-κB途径改变有关。

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