Cell Killing by Reovirus: Mechanisms and Consequences.

3区 医学 Q2 Medicine
Andrew McNamara, Katherine Roebke, Pranav Danthi
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引用次数: 3

Abstract

Infection of host cells by mammalian reovirus in culture or in tissues of infected animals results in cell death. Cell death of infected neurons and myocytes contributes to the pathogenesis of reovirus-induced encephalitis and myocarditis in a newborn mouse model. Thus, reovirus-induced cell death has been used to investigate the basis of viral disease. Depending on the cell type, infection of host cells by reovirus results in one of two forms of cell death-apoptosis and necroptosis. In addition to the obvious differences in how these two forms of cell death are executed, the mechanisms by which reovirus infection initiates and transduces signals that lead to each of these types of cell death are distinct. In this review, we discuss how apoptosis and necroptosis are triggered by events at different stages of infection. We also describe how innate immune recognition of reovirus genomic material and type I interferon signaling pathways connect with the core components of the apoptosis and necroptosis machinery. The impact of different cell death mediators on viral pathogenesis and the potential of reovirus as an oncolytic vector are also outlined.

Reovirus 杀死细胞:机制与后果
哺乳动物雷诺病毒在培养液中或感染动物的组织中感染宿主细胞会导致细胞死亡。在新生小鼠模型中,受感染神经元和心肌细胞的细胞死亡是再病毒诱发脑炎和心肌炎的发病机制之一。因此,再病毒诱导的细胞死亡已被用于研究病毒性疾病的基础。根据细胞类型的不同,宿主细胞感染雷诺病毒后会导致两种形式的细胞死亡--细胞凋亡和坏死。除了这两种细胞死亡形式的执行方式存在明显差异外,重组病毒感染启动和传递导致这两种细胞死亡的信号的机制也各不相同。在本综述中,我们将讨论细胞凋亡和坏死是如何在感染的不同阶段被触发的。我们还描述了先天性免疫对重组病毒基因组材料的识别和 I 型干扰素信号通路如何与细胞凋亡和坏死机制的核心组成部分相联系。我们还概述了不同细胞死亡介质对病毒发病机制的影响,以及重组病毒作为溶瘤载体的潜力。
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来源期刊
CiteScore
5.60
自引率
0.00%
发文量
26
审稿时长
>12 weeks
期刊介绍: The review series Current Topics in Microbiology and Immunology provides a synthesis of the latest research findings in the areas of molecular immunology, bacteriology and virology. Each timely volume contains a wealth of information on the featured subject. This review series is designed to provide access to up-to-date, often previously unpublished information.
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