深入了解由变形病毒介导的自噬和凋亡的不同机制。

Rashmi Singh, Sharad Kumar Gaur, Rakhi Nagar, Rajeev Kaul
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引用次数: 0

摘要

病毒是与宿主共同进化的专性细胞内寄生虫。在进化过程中,病毒通过调节宿主蛋白获得了消除宿主免疫反应的能力,而宿主蛋白在各种生物过程中起着关键作用。其中一个过程是病毒感染细胞的程序性细胞死亡,它可以通过自噬或凋亡发生。已知麻疹病毒可调节自噬和细胞凋亡。在感染细胞后,麻疹病毒可以利用自噬体作为巢穴,延缓宿主防御凋亡反应,或促进细胞凋亡,使病毒传播升级。此外,这两种途径之间存在积极的相互作用,最终决定了病毒感染细胞的命运。我们对这些过程的理解的最新进展为进一步探索麻疹病毒的治疗目的提供了潜在的理论基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Insights into the different mechanisms of Autophagy and Apoptosis mediated by Morbilliviruses.

Viruses are obligate intracellular parasites that have co-evolved with the host. During the course of evolution, viruses have acquired abilities to abrogate the host's immune responses by modulating the host proteins which play a pivotal role in various biological processes. One such process is the programmed cell death in virus-infected cells, which can occur via autophagy or apoptosis. Morbilliviruses are known to modulate both autophagy and apoptosis. Upon infecting a cell, the morbilliviruses can utilize autophagosomes as their nest and delay the host defense apoptotic response, and/or can promote apoptosis to escalate the virus dissemination. Moreover, there is an active interplay between these two pathways which eventually decides the fate of a virus-infected cell. Recent advances in our understanding of these processes provide a potential rationale to further explore morbilliviruses for therapeutic purposes.

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