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丝状病毒逃避抗病毒反应的策略。

Filovirus Strategies to Escape Antiviral Responses.

机构信息

Department of Microbiology and National Emerging Infectious Diseases Laboratories, Boston University School of Medicine, 620 Albany Street, Boston, MA, 02118, USA.

Department of Pathology and Immunology, Washington University School of Medicine in St. Louis, St. Louis, MO, 63110, USA.

出版信息

Curr Top Microbiol Immunol. 2017;411:293-322. doi: 10.1007/82_2017_13.

DOI:10.1007/82_2017_13
PMID:28685291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5973841/
Abstract

This chapter describes the various strategies filoviruses use to escape host immune responses with a focus on innate immune and cell death pathways. Since filovirus replication can be efficiently blocked by interferon (IFN), filoviruses have evolved mechanisms to counteract both type I IFN induction and IFN response signaling pathways. Intriguingly, marburg- and ebolaviruses use different strategies to inhibit IFN signaling. This chapter also summarizes what is known about the role of IFN-stimulated genes (ISGs) in filovirus infection. These fall into three categories: those that restrict filovirus replication, those whose activation is inhibited by filoviruses, and those that have no measurable effect on viral replication. In addition to innate immunity, mammalian cells have evolved strategies to counter viral infections, including the induction of cell death and stress response pathways, and we summarize our current knowledge of how filoviruses interact with these pathways. Finally, this chapter delves into the interaction of EBOV with myeloid dendritic cells and macrophages and the associated inflammatory response, which differs dramatically between these cell types when they are infected with EBOV. In summary, we highlight the multifaceted nature of the host-viral interactions during filoviral infections.

摘要

本章描述了丝状病毒逃避宿主免疫反应的各种策略,重点介绍了先天免疫和细胞死亡途径。由于丝状病毒的复制可以被干扰素 (IFN) 有效地阻断,因此丝状病毒已经进化出了对抗 I 型 IFN 诱导和 IFN 反应信号通路的机制。有趣的是,马尔堡病毒和埃博拉病毒使用不同的策略来抑制 IFN 信号。本章还总结了 IFN 刺激基因 (ISGs) 在丝状病毒感染中的作用。这些基因分为三类:限制丝状病毒复制的基因、被丝状病毒抑制激活的基因,以及对病毒复制没有可测量影响的基因。除了先天免疫,哺乳动物细胞还进化出了对抗病毒感染的策略,包括诱导细胞死亡和应激反应途径,我们总结了我们目前对丝状病毒与这些途径相互作用的了解。最后,本章深入探讨了 EBOV 与髓样树突状细胞和巨噬细胞的相互作用以及相关的炎症反应,当这两种细胞类型被 EBOV 感染时,它们的反应存在显著差异。总之,我们强调了丝状病毒感染期间宿主-病毒相互作用的多方面性质。

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本文引用的文献

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Ebolaviruses Associated with Differential Pathogenicity Induce Distinct Host Responses in Human Macrophages.与不同致病性相关的埃博拉病毒在人类巨噬细胞中引发不同的宿主反应。
J Virol. 2017 May 12;91(11). doi: 10.1128/JVI.00179-17. Print 2017 Jun 1.
2
Ebola virus VP35 blocks stress granule assembly.埃博拉病毒VP35蛋白可阻止应激颗粒的组装。
Virology. 2017 Feb;502:73-83. doi: 10.1016/j.virol.2016.12.012. Epub 2016 Dec 23.
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A hamster model for Marburg virus infection accurately recapitulates Marburg hemorrhagic fever.一种用于马尔堡病毒感染的仓鼠模型准确再现了马尔堡出血热。
Sci Rep. 2016 Dec 15;6:39214. doi: 10.1038/srep39214.
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VP24-Karyopherin Alpha Binding Affinities Differ between Ebolavirus Species, Influencing Interferon Inhibition and VP24 Stability.埃博拉病毒不同物种之间的VP24-核转运蛋白α结合亲和力存在差异,影响干扰素抑制作用和VP24稳定性。
J Virol. 2017 Jan 31;91(4). doi: 10.1128/JVI.01715-16. Print 2017 Feb 15.
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Novel activities by ebolavirus and marburgvirus interferon antagonists revealed using a standardized in vitro reporter system.使用标准化体外报告系统揭示埃博拉病毒和马尔堡病毒干扰素拮抗剂的新活性。
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The Ebola Interferon Inhibiting Domains Attenuate and Dysregulate Cell-Mediated Immune Responses.埃博拉干扰素抑制结构域会减弱并失调细胞介导的免疫反应。
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In vivo Ebola virus infection leads to a strong innate response in circulating immune cells.体内埃博拉病毒感染会导致循环免疫细胞产生强烈的先天性反应。
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Dimerization Controls Marburg Virus VP24-dependent Modulation of Host Antioxidative Stress Responses.二聚化调控马尔堡病毒VP24介导的宿主抗氧化应激反应调节
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