Immunopathogenesis and Virus-Host Interactions of Enterovirus 71 in Patients with Hand, Foot and Mouth Disease.

Immunopathogenesis and Virus-Host Interactions of Enterovirus 71 in Patients with Hand, Foot and Mouth Disease.
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DOI:
10.3389/fmicb.2017.02249
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发表时间:
2017
影响因子:
5.2
通讯作者:
Ng LFP
Ng LFP
中科院分区:
生物学2区
文献类型:
--
作者:
Cox JA;Hiscox JA;Solomon T;Ooi MH;Ng LFP

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肠道病毒71(EV 71)是一种全球性传染病,影响数百万人。该病毒是手足口病的主要病原体,在全球范围内报告了暴发和流行。感染可导致5岁以下儿童出现严重的神经、心脏和呼吸问题。尽管不断努力,但对EV 71的发病机制、宿主免疫系统如何对病毒作出反应以及这些反应背后的分子机制知之甚少。此外,目前的动物模型仍然有限,因为它们不能重现在人类中观察到的类似疾病模式和症状。在这篇综述中,EV 71的宿主-病毒相互作用的作用进行了讨论,连同各种模型可用于检查:EV 71如何利用其蛋白质切割宿主因子和蛋白质,帮助病毒复制; EV 71如何使用自己的病毒蛋白质破坏宿主的免疫反应,并帮助其免疫逃避。这些发现沿着其他发现,如EV 71晶体结构,为治疗和药物干预提供了可能的靶点。
Enterovirus 71 (EV71) is a global infectious disease that affects millions of people. The virus is the main etiological agent for hand, foot, and mouth disease with outbreaks and epidemics being reported globally. Infection can cause severe neurological, cardiac, and respiratory problems in children under the age of 5. Despite on-going efforts, little is known about the pathogenesis of EV71, how the host immune system responds to the virus and the molecular mechanisms behind these responses. Moreover, current animal models remain limited, because they do not recapitulate similar disease patterns and symptoms observed in humans. In this review the role of the host–viral interactions of EV71 are discussed together with the various models available to examine: how EV71 utilizes its proteins to cleave host factors and proteins, aiding virus replication; how EV71 uses its own viral proteins to disrupt host immune responses and aid in its immune evasion. These discoveries along with others, such as the EV71 crystal structure, have provided possible targets for treatment and drug interventions.
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