Suppr超能文献

非死即生:病毒对细胞凋亡的逃避

To kill or be killed: viral evasion of apoptosis.

作者信息

Benedict Chris A, Norris Paula S, Ware Carl F

机构信息

Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.

出版信息

Nat Immunol. 2002 Nov;3(11):1013-8. doi: 10.1038/ni1102-1013.

Abstract

In the struggle between virus and host, control over the cell's death machinery is crucial for survival. Viruses are obligatory intracellular parasites and, as such, must modulate apoptotic pathways to control the lifespan of their host in order to complete their replication cycle. Many of the counter-assaults mounted by the immune system incorporate activation of the apoptotic pathway-particularly by members of the tumor necrosis factor cytokine family-as a mechanism to restrict viral replication. Thus, apoptosis serves as a powerful selective pressure for the virus to evade. However, for the host, success is harsh and potentially costly, as apoptosis often contributes to pathogenesis. Here we examine some of the molecular mechanisms by which viruses manipulate the apoptotic machinery to their advantage and how we (as vertebrates) have evolved and learned to cope with viral evasion.

摘要

在病毒与宿主的斗争中,对细胞死亡机制的控制对于生存至关重要。病毒是 obligatory 细胞内寄生虫,因此,必须调节凋亡途径以控制其宿主的寿命,以便完成其复制周期。免疫系统发起的许多反击都包括激活凋亡途径——特别是通过肿瘤坏死因子细胞因子家族的成员——作为限制病毒复制的一种机制。因此,凋亡成为病毒逃避的强大选择压力。然而,对于宿主来说,成功是严酷的且可能代价高昂,因为凋亡常常导致发病机制。在这里,我们研究了病毒利用凋亡机制为自身谋利的一些分子机制,以及我们(作为脊椎动物)是如何进化并学会应对病毒逃避的。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验