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Attenuated and lethal variants of Pichindé virus induce differential patterns of NF-kappaB activation suggesting a potential target for novel therapeutics.皮钦德病毒的减毒和致死变体诱导不同的 NF-κB 激活模式，提示了一种新型治疗药物的潜在靶点。
Viral Immunol. 2009 Dec;22(6):457-62. doi: 10.1089/vim.2009.0034.
2
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
J Virol. 2002 Feb;76(3):1154-62. doi: 10.1128/jvi.76.3.1154-1162.2002.
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Bovine glycomacropeptide induces cytokine production in human monocytes through the stimulation of the MAPK and the NF-kappaB signal transduction pathways.牛糖巨肽通过刺激 MAPK 和 NF-κB 信号转导通路诱导人单核细胞产生细胞因子。
Br J Pharmacol. 2009 Aug;157(7):1232-40. doi: 10.1111/j.1476-5381.2009.00195.x. Epub 2009 Jun 22.
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Activation of nuclear transcription factor-kappa B is associated with the induction of inhibitory kappa B kinase-beta and involves differential activation of protein kinase C and protein tyrosine kinases during fatal murine cerebral malaria.核转录因子-κB的激活与抑制性κB激酶-β的诱导相关，并且在致命性小鼠脑型疟疾期间涉及蛋白激酶C和蛋白酪氨酸激酶的差异激活。
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Src tyrosine kinases mediate crystalline silica-induced NF-kappaB activation through tyrosine phosphorylation of IkappaB-alpha and p65 NF-kappaB in RAW 264.7 macrophages.Src酪氨酸激酶通过在RAW 264.7巨噬细胞中使IκB-α和p65 NF-κB发生酪氨酸磷酸化，介导结晶二氧化硅诱导的NF-κB激活。
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Activation of NF-kappaB by fluid shear stress, but not TNF-alpha, requires focal adhesion kinase in osteoblasts.流体切应力而非 TNF-α 通过黏着斑激酶激活成骨细胞中的 NF-κB。
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The tumor suppressor Sef is a scaffold for the classical NF-κB/RELA:P50 signaling module.肿瘤抑制因子 Sef 是经典 NF-κB/RELA:P50 信号模块的支架。
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IKKbeta programs to turn on the GADD45alpha-MKK4-JNK apoptotic cascade specifically via p50 NF-kappaB in arsenite response.在亚砷酸盐反应中，IKKβ 专门通过 p50 NF-κB 开启 GADD45α-MKK4-JNK 凋亡级联反应。
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Ultraviolet B radiation activates NF-κB and induces iNOS expression in HR-1 hairless mouse skin: role of IκB kinase-β.中波紫外线辐射激活 NF-κB 并诱导 HR-1 无毛小鼠皮肤中 iNOS 的表达：IKK-β 的作用。
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引用本文的文献

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Innate immune response to arenaviral infection: a focus on the highly pathogenic New World hemorrhagic arenaviruses.天然免疫对沙粒病毒感染的应答：关注高致病性新域出血沙粒病毒。
J Mol Biol. 2013 Dec 13;425(24):4893-903. doi: 10.1016/j.jmb.2013.09.028. Epub 2013 Sep 26.
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An attenuated Lassa vaccine in SIV-infected rhesus macaques does not persist or cause arenavirus disease but does elicit Lassa virus-specific immunity.感染 SIV 的恒河猴中减毒的拉萨病毒疫苗不能持续存在或引起沙粒病毒病，但能引起拉萨病毒特异性免疫。
Virol J. 2013 Feb 12;10:52. doi: 10.1186/1743-422X-10-52.
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A systems biology starter kit for arenaviruses.沙粒病毒系统生物学入门工具包
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The search for animal models for Lassa fever vaccine development.拉沙热疫苗开发的动物模型研究。
Expert Rev Vaccines. 2013 Jan;12(1):71-86. doi: 10.1586/erv.12.139.
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Arenavirus nucleoproteins prevent activation of nuclear factor kappa B.沙粒病毒核蛋白可阻止核因子 κB 的激活。
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Meta-analysis of high-throughput datasets reveals cellular responses following hemorrhagic fever virus infection.高通量数据集的荟萃分析揭示了出血热病毒感染后的细胞反应。
Viruses. 2011 May;3(5):613-9. doi: 10.3390/v3050613. Epub 2011 May 12.
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Vaccine and adjuvant design for emerging viruses: mutations, deletions, segments and signaling.新兴病毒的疫苗和佐剂设计：突变、缺失、片段与信号传导
Bioeng Bugs. 2011 May-Jun;2(3):129-35. doi: 10.4161/bbug.2.3.15367. Epub 2011 May 1.
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Interference with intraepithelial TNF-α signaling inhibits CD8(+) T-cell-mediated lung injury in influenza infection.干扰上皮内 TNF-α 信号传导可抑制流感感染中 CD8(+) T 细胞介导的肺损伤。
Viral Immunol. 2010 Dec;23(6):639-45. doi: 10.1089/vim.2010.0076.
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Proteomic analysis of Pichindé virus infection identifies differential expression of prothymosin-alpha.皮钦德病毒感染的蛋白质组学分析确定了胸腺素α原的差异表达。
J Biomed Biotechnol. 2010;2010. doi: 10.1155/2010/956823. Epub 2010 Apr 18.
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Comparative pathogenesis and systems biology for biodefense virus vaccine development.用于生物防御病毒疫苗开发的比较发病机制与系统生物学
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本文引用的文献

1
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。
Future Virol. 2008;3(3):243-251. doi: 10.2217/17460794.3.3.243.
2
Gene expression in primate liver during viral hemorrhagic fever.病毒性出血热期间灵长类动物肝脏中的基因表达。
Virol J. 2009 Feb 12;6:20. doi: 10.1186/1743-422X-6-20.
3
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。
J Virol. 2009 Jan;83(2):687-700. doi: 10.1128/JVI.01281-08. Epub 2008 Nov 12.
4
Genistein treatment of cells inhibits arenavirus infection.金雀异黄素对细胞的处理可抑制沙粒病毒感染。
Antiviral Res. 2008 Feb;77(2):153-6. doi: 10.1016/j.antiviral.2007.09.005. Epub 2007 Oct 8.
5
Differential inhibition of type I interferon induction by arenavirus nucleoproteins.沙粒病毒核蛋白对I型干扰素诱导的差异性抑制作用。
J Virol. 2007 Nov;81(22):12696-703. doi: 10.1128/JVI.00882-07. Epub 2007 Sep 5.
6
Early blood profiles of virus infection in a monkey model for Lassa fever.拉沙热猴模型中病毒感染的早期血液特征
J Virol. 2007 Aug;81(15):7960-73. doi: 10.1128/JVI.00536-07. Epub 2007 May 23.
7
Beyond IkappaBs: alternative regulation of NF-kappaB activity.超越IκB蛋白：核因子-κB活性的其他调控方式
FASEB J. 2007 Sep;21(11):2642-54. doi: 10.1096/fj.06-7615rev. Epub 2007 Apr 12.
8
Thioaptamer decoy targeting of AP-1 proteins influences cytokine expression and the outcome of arenavirus infections.靶向 AP-1 蛋白的硫适配体诱饵影响细胞因子表达和沙粒病毒感染的结果。
J Gen Virol. 2007 Mar;88(Pt 3):981-990. doi: 10.1099/vir.0.82499-0.
9
Identification of differentially activated cell-signaling networks associated with pichinde virus pathogenesis by using systems kinomics.运用系统激酶组学鉴定与皮钦德病毒发病机制相关的差异激活细胞信号网络。
J Virol. 2007 Feb;81(4):1923-33. doi: 10.1128/JVI.02199-06. Epub 2006 Dec 6.
10
Post-translational modifications regulating the activity and function of the nuclear factor kappa B pathway.调节核因子κB信号通路活性和功能的翻译后修饰
Oncogene. 2006 Oct 30;25(51):6717-30. doi: 10.1038/sj.onc.1209937.

皮钦德病毒的减毒和致死变体诱导不同的 NF-κB 激活模式，提示了一种新型治疗药物的潜在靶点。

Attenuated and lethal variants of Pichindé virus induce differential patterns of NF-kappaB activation suggesting a potential target for novel therapeutics.

机构信息

Center for Biodefense and Emerging Infectious Diseases, University of Texas Medical Branch, Galveston, Texas 77555-0609, USA.

出版信息

Viral Immunol. 2009 Dec;22(6):457-62. doi: 10.1089/vim.2009.0034.

DOI:10.1089/vim.2009.0034
PMID:19951183
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2883487/
Abstract

Lassa virus pathogenesis is believed to involve dysregulation of cytokines. We have previously shown nuclear factor-kappaB (NF-kappaB) inhibition using a BSL-2 model for Lassa fever. Here we further define the potential mechanism for NF-kappaB inhibition as involving increased levels of repressive p50/p50 homodimers, and suggest a novel therapeutic strategy that acts via modulation of host signaling.

摘要

拉沙病毒发病机制被认为涉及细胞因子失调。我们之前已经在拉沙热的 BSL-2 模型中展示了使用核因子-κB（NF-κB）抑制剂。在这里，我们进一步定义了 NF-κB 抑制的潜在机制，涉及增加抑制性 p50/p50 同源二聚体的水平，并提出了一种通过调节宿主信号转导发挥作用的新型治疗策略。