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Biochemical and functional characterization of the membrane association and membrane permeabilizing activity of the severe acute respiratory syndrome coronavirus envelope protein.严重急性呼吸综合征冠状病毒包膜蛋白的膜结合及膜通透活性的生化与功能特性
Virology. 2006 Jun 5;349(2):264-75. doi: 10.1016/j.virol.2006.01.028. Epub 2006 Feb 28.
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p38 mitogen-activated protein kinase-dependent hyperinduction of tumor necrosis factor alpha expression in response to avian influenza virus H5N1.p38丝裂原活化蛋白激酶依赖性肿瘤坏死因子α表达在应对禽流感病毒H5N1时的过度诱导
J Virol. 2005 Aug;79(16):10147-54. doi: 10.1128/JVI.79.16.10147-10154.2005.
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Mutagenesis of the murine hepatitis virus nsp1-coding region identifies residues important for protein processing, viral RNA synthesis, and viral replication.鼠肝炎病毒nsp1编码区的诱变鉴定出对蛋白质加工、病毒RNA合成和病毒复制重要的残基。
Virology. 2005 Sep 30;340(2):209-23. doi: 10.1016/j.virol.2005.06.035.
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Cytokine responses in severe acute respiratory syndrome coronavirus-infected macrophages in vitro: possible relevance to pathogenesis.体外严重急性呼吸综合征冠状病毒感染巨噬细胞中的细胞因子反应：与发病机制的可能关联
J Virol. 2005 Jun;79(12):7819-26. doi: 10.1128/JVI.79.12.7819-7826.2005.
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Mechanisms for HIV Tat upregulation of IL-10 and other cytokine expression: kinase signaling and PKR-mediated immune response.HIV反式激活因子上调白细胞介素-10及其他细胞因子表达的机制：激酶信号传导与蛋白激酶R介导的免疫反应。
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Chemokine up-regulation in SARS-coronavirus-infected, monocyte-derived human dendritic cells.严重急性呼吸综合征冠状病毒感染的人单核细胞来源树突状细胞中趋化因子的上调
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Differential maturation and subcellular localization of severe acute respiratory syndrome coronavirus surface proteins S, M and E.严重急性呼吸综合征冠状病毒表面蛋白S、M和E的差异成熟及亚细胞定位
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Characterization of viral proteins encoded by the SARS-coronavirus genome.严重急性呼吸综合征冠状病毒基因组编码的病毒蛋白的特性分析
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Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome.严重急性呼吸综合征细胞因子/趋化因子谱的特征分析
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10
High-dose hydrocortisone reduces expression of the pro-inflammatory chemokines CXCL8 and CXCL10 in SARS coronavirus-infected intestinal cells.大剂量氢化可的松可降低严重急性呼吸综合征冠状病毒感染的肠道细胞中促炎趋化因子CXCL8和CXCL10的表达。
Int J Mol Med. 2005 Feb;15(2):323-7.

严重急性呼吸综合征冠状病毒非结构蛋白1在趋化因子失调中的作用

Role for nonstructural protein 1 of severe acute respiratory syndrome coronavirus in chemokine dysregulation.

作者信息

Law Anna H Y, Lee Davy C W, Cheung Benny K W, Yim Howard C H, Lau Allan S Y

机构信息

Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Pokfulam, Hong Kong, Special Administrative Region, China.

出版信息

J Virol. 2007 Jan;81(1):416-22. doi: 10.1128/JVI.02336-05. Epub 2006 Oct 11.

DOI:10.1128/JVI.02336-05
PMID:17035307
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1797241/
Abstract

Severe acute respiratory syndrome (SARS) is an emerging infectious disease caused by a novel coronavirus. Since its associated morbidity and mortality have been postulated to be due to immune dysregulation, we investigated which of the viral proteins is responsible for chemokine overexpression. To delineate the viral and cellular factor interactions, the role of four SARS coronavirus proteins, including nonstructural protein 1 (nsp-1), nsp-5, envelope, and membrane, were examined in terms of cytokine induction. Our results showed that the SARS coronavirus nsp-1 plays an important role in CCL5, CXCL10, and CCL3 expression in human lung epithelial cells via the activation of NF-kappaB.

摘要

严重急性呼吸综合征（SARS）是一种由新型冠状病毒引起的新发传染病。鉴于其相关的发病率和死亡率被认为是由于免疫失调所致，我们研究了哪种病毒蛋白导致趋化因子过度表达。为了阐明病毒与细胞因子的相互作用，我们从细胞因子诱导方面研究了四种严重急性呼吸综合征冠状病毒蛋白的作用，包括非结构蛋白1（nsp-1）、nsp-5、包膜蛋白和膜蛋白。我们的结果表明，严重急性呼吸综合征冠状病毒nsp-1通过激活核因子κB在人肺上皮细胞中CCL5、CXCL10和CCL3的表达中发挥重要作用。