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Differential signaling networks induced by mild and lethal hemorrhagic fever virus infections.轻度和致死性出血热病毒感染诱导的差异信号网络。
J Virol. 2006 Oct;80(20):10248-52. doi: 10.1128/JVI.01384-06.
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Molecular determinants of Pichinde virus infection of guinea pigs--a small animal model system for arenaviral hemorrhagic fevers.皮钦德病毒感染豚鼠的分子决定因素——一种用于沙粒病毒出血热的小动物模型系统
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Analysis of the differential host cell nuclear proteome induced by attenuated and virulent hemorrhagic arenavirus infection.减毒和强毒出血性沙粒病毒感染诱导的宿主细胞核差异蛋白质组分析。
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Virology. 2001 Nov 10;290(1):30-8. doi: 10.1006/viro.2001.1127.
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In vitro and in vivo characterizations of pichinde viral nucleoprotein exoribonuclease functions.皮钦德病毒核蛋白外切核糖核酸酶功能的体外和体内表征
J Virol. 2015 Jul;89(13):6595-607. doi: 10.1128/JVI.00009-15. Epub 2015 Apr 15.

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Neuroretinal degeneration in a mouse model of systemic chronic immune activation observed by proteomics.通过蛋白质组学观察到系统性慢性免疫激活小鼠模型中的神经视网膜变性。
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Virulent infection of outbred Hartley guinea pigs with recombinant Pichinde virus as a surrogate small animal model for human Lassa fever.用重组皮钦德病毒对杂种 Hartley 豚鼠进行烈性感染,作为人类拉沙热的替代小动物模型。
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Expression of interferon-induced antiviral genes is delayed in a STAT1 knockout mouse model of Crimean-Congo hemorrhagic fever.干扰素诱导的抗病毒基因在克里米亚-刚果出血热的 STAT1 敲除小鼠模型中表达延迟。
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Exploring kinase inhibitors as therapies for human arenavirus infections.探索激酶抑制剂作为治疗人类沙粒病毒感染的方法。
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本文引用的文献

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A network-based analysis of systemic inflammation in humans.基于网络的人类全身炎症分析。
Nature. 2005 Oct 13;437(7061):1032-7. doi: 10.1038/nature03985. Epub 2005 Aug 31.
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TNF-related activation-induced cytokine enhances leukocyte adhesiveness: induction of ICAM-1 and VCAM-1 via TNF receptor-associated factor and protein kinase C-dependent NF-kappaB activation in endothelial cells.肿瘤坏死因子相关激活诱导细胞因子增强白细胞黏附性:通过肿瘤坏死因子受体相关因子及蛋白激酶C依赖的核因子κB激活在内皮细胞中诱导细胞间黏附分子-1和血管细胞黏附分子-1。
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p53 is a suppressor of inflammatory response in mice.p53是小鼠炎症反应的抑制因子。
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Human macrophages, but not dendritic cells, are activated and produce alpha/beta interferons in response to Mopeia virus infection.人类巨噬细胞而非树突状细胞,在受到莫佩亚病毒感染时会被激活并产生α/β干扰素。
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Lassa virus infection of human dendritic cells and macrophages is productive but fails to activate cells.拉沙病毒对人树突状细胞和巨噬细胞的感染具有增殖性,但无法激活这些细胞。
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Cutting edge: impairment of dendritic cells and adaptive immunity by Ebola and Lassa viruses.前沿:埃博拉病毒和拉沙病毒对树突状细胞及适应性免疫的损害
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The inflammatory reflex.炎症反射。
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Alterations in NF-kappaB and RBP-Jkappa by arenavirus infection of macrophages in vitro and in vivo.体外和体内巨噬细胞受沙粒病毒感染后NF-κB和RBP-Jκ的变化
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NF-kappaB/RelA transactivation is required for atypical protein kinase C iota-mediated cell survival.非典型蛋白激酶C ι介导的细胞存活需要核因子-κB/RelA反式激活。
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Glycogen synthase kinase3 beta phosphorylates serine 33 of p53 and activates p53's transcriptional activity.糖原合酶激酶3β使p53的丝氨酸33磷酸化并激活p53的转录活性。
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轻度和致死性出血热病毒感染诱导的差异信号网络。

Differential signaling networks induced by mild and lethal hemorrhagic fever virus infections.

作者信息

Bowick Gavin C, Fennewald Susan M, Elsom Barry L, Aronson Judith F, Luxon Bruce A, Gorenstein David G, Herzog Norbert K

机构信息

University of Texas Medical Branch, 201 University Blvd., Galveston, TX 77555, USA.

出版信息

J Virol. 2006 Oct;80(20):10248-52. doi: 10.1128/JVI.01384-06.

DOI:10.1128/JVI.01384-06
PMID:17005702
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1617297/
Abstract

The family Arenaviridae includes several National Institutes of Allergy and Infections Diseases category A select agents which cause hemorrhagic fever. There are few vaccines available, and treatment is limited to ribavirin, which varies in efficacy. Development of new antiviral compounds has been hindered by a lack of understanding of the molecular basis of pathogenesis. We used two variants of Pichinde virus, one attenuated and one virulent in the guinea pig model, to delineate the host determinants which lead to either viral clearance or lethal disease. By analyzing protein level changes using pathway analysis, we have identified key intermediates which may be targets for therapeutic intervention.

摘要

沙粒病毒科包含几种美国国立过敏与传染病研究所指定的A类生物制剂,可引发出血热。可用的疫苗很少,治疗仅限于利巴韦林,其疗效各异。由于对发病机制的分子基础缺乏了解,新型抗病毒化合物的研发受到了阻碍。我们使用了皮钦德病毒的两种变体,一种在豚鼠模型中减毒,另一种具有毒性,以确定导致病毒清除或致死性疾病的宿主决定因素。通过使用通路分析来分析蛋白质水平的变化,我们确定了可能成为治疗干预靶点的关键中间体。