Cell Killing by Reovirus: Mechanisms and Consequences.
Cell Killing by Reovirus: Mechanisms and Consequences.
复制标题
呼肠孤病毒杀死细胞：机制和后果。
DOI：
10.1007/82_2020_225
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发表时间：
2023
影响因子：
--
通讯作者：
Danthi,Pranav
中科院分区：
文献类型：
--
作者：
McNamara,Andrew;Roebke,Katherine;Danthi,Pranav
哺乳动物呼肠孤病毒在培养物或感染动物的组织中感染宿主细胞导致细胞死亡。在新生小鼠模型中，受感染的神经元和肌细胞的细胞死亡有助于呼肠孤病毒诱导的脑炎和心肌炎的发病机制。因此，呼肠孤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，呼肠孤病毒感染宿主细胞导致两种形式的细胞死亡-细胞凋亡和坏死性凋亡。除了这两种形式的细胞死亡如何执行的明显差异之外，呼肠孤病毒感染引发和转导导致每种类型细胞死亡的信号的机制也是不同的。在这篇综述中，我们讨论了细胞凋亡和坏死性凋亡是如何在感染的不同阶段触发的事件。我们还描述了呼肠孤病毒基因组物质和I型干扰素信号通路的先天免疫识别如何与细胞凋亡和坏死性凋亡机制的核心组成部分连接。不同的细胞死亡介质对病毒的发病机制和呼肠孤病毒作为溶瘤载体的潜力的影响也进行了概述。
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.
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影响因子：
30.3
作者：
Thapa RJ;Ingram JP;Ragan KB;Nogusa S;Boyd DF;Benitez AA;Sridharan H;Kosoff R;Shubina M;Landsteiner VJ;Andrake M;Vogel P;Sigal LJ;tenOever BR;Thomas PG;Upton JW;Balachandran S
通讯作者：
Balachandran S
影响因子：
11.2
作者：
Thirukkumaran, Chandini M.;Nodwell, Michael J.;Morris, Don G.
通讯作者：
Morris, Don G.
影响因子：
5.4
作者：
Murray, Kenneth E.;Nibert, Max L.
通讯作者：
Nibert, Max L.
呼肠孤病毒毒力的分子基础：S1 基因的作用。
DOI：
10.1073/pnas.74.12.5744
发表时间：
1977
影响因子：
11.1
作者：
H. Weiner;D. Drayna;D. Averill;B. Fields
通讯作者：
B. Fields
致癌 Ras 通过 RIG-I 信号传导的负调节抑制 IFN-β 的产生，从而促进呼肠孤病毒传播。
影响因子：
11.2
作者：
M. Shmulevitz;L. Pan;Katy A. Garant;D. Pan;Patrick Lee
通讯作者：
Patrick Lee