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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
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JNK and PI3k/Akt signaling pathways are required for establishing persistent SARS-CoV infection in Vero E6 cells.在Vero E6细胞中建立持续性严重急性呼吸综合征冠状病毒（SARS-CoV）感染需要JNK和PI3k/Akt信号通路。
Biochim Biophys Acta. 2005 Jun 30;1741(1-2):4-10. doi: 10.1016/j.bbadis.2005.04.004.
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Microarray and real-time RT-PCR analyses of differential human gene expression patterns induced by severe acute respiratory syndrome (SARS) coronavirus infection of Vero cells.对严重急性呼吸综合征（SARS）冠状病毒感染Vero细胞所诱导的人类基因差异表达模式的微阵列和实时逆转录聚合酶链反应分析。
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Subcellular localization and membrane association of SARS-CoV 3a protein.严重急性呼吸综合征冠状病毒3a蛋白的亚细胞定位及与膜的关联
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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。
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An interferon-gamma-related cytokine storm in SARS patients.SARS患者中与干扰素-γ相关的细胞因子风暴。
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Induction of IL-8 release in lung cells via activator protein-1 by recombinant baculovirus displaying severe acute respiratory syndrome-coronavirus spike proteins: identification of two functional regions.通过展示严重急性呼吸综合征冠状病毒刺突蛋白的重组杆状病毒经激活蛋白-1诱导肺细胞释放白细胞介素-8：两个功能区域的鉴定
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Overexpression of 7a, a protein specifically encoded by the severe acute respiratory syndrome coronavirus, induces apoptosis via a caspase-dependent pathway.严重急性呼吸综合征冠状病毒特异性编码的蛋白质7a的过表达通过半胱天冬酶依赖性途径诱导细胞凋亡。
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Tyrosine dephosphorylation of STAT3 in SARS coronavirus-infected Vero E6 cells.严重急性呼吸综合征冠状病毒感染的非洲绿猴肾细胞中信号转导子和转录激活子3的酪氨酸去磷酸化作用
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严重急性呼吸综合征冠状病毒（SARS-CoV）感染细胞中的信号转导

Signal transduction in SARS-CoV-infected cells.

作者信息

Mizutani T

机构信息

Department of Virology 1, National Institute of Infectious Diseases, Gakuen 4-7-1, Musashimurayama, Tokyo, Japan.

出版信息

Ann N Y Acad Sci. 2007 Apr;1102(1):86-95. doi: 10.1196/annals.1408.006.

DOI:10.1196/annals.1408.006
PMID:17470913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7167675/
Abstract

Severe acute respiratory syndrome (SARS) is a newly found infectious disease that is caused by a novel human coronavirus, SARS coronavirus (SARS-CoV). Because the mortality rate of SARS patients is very high, understanding the pathological mechanisms of SARS not only in vivo but in vitro is important for the prevention of SARS. Activation of signaling pathways caused by SARS-CoV infection leads to the phosphorylation and activation of downstream molecules. Two conflicting cellular programs, apoptosis to eliminate virus-infected cells and survival to delay apoptosis by producing antiviral cytokines, occur in SARS patients. Recent studies regarding SARS and SARS-CoV have clarified that activation of mitogen-activated protein kinases (MAPKs) plays important roles in upregulation of cytokine expression and apoptosis both in vitro and in vivo. Both Akt and p38 MAPK are keys for determination of cell survival or death in SARS-CoV-infected cells in vitro. Agents being developed to target these signaling cascades may be important for the design of anti-SARS-CoV drugs. This review highlights recent progress regarding SARS-CoV biology, especially signal transduction in SARS-CoV-infected cells.

摘要

严重急性呼吸综合征（SARS）是一种新发现的传染病，由一种新型人类冠状病毒——SARS冠状病毒（SARS-CoV）引起。由于SARS患者的死亡率很高，了解SARS在体内和体外的病理机制对于预防SARS至关重要。SARS-CoV感染引起的信号通路激活导致下游分子的磷酸化和激活。在SARS患者中出现了两个相互冲突的细胞程序，即通过凋亡清除病毒感染细胞和通过产生抗病毒细胞因子延缓凋亡以存活。最近关于SARS和SARS-CoV的研究表明，丝裂原活化蛋白激酶（MAPKs）的激活在体外和体内细胞因子表达上调和凋亡中均起重要作用。Akt和p38 MAPK都是体外SARS-CoV感染细胞中决定细胞存活或死亡的关键因素。针对这些信号级联开发的药物可能对设计抗SARS-CoV药物很重要。本综述重点介绍了SARS-CoV生物学的最新进展，特别是SARS-CoV感染细胞中的信号转导。