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Effects of Cell Proteostasis Network on the Survival of SARS-CoV-2
Biological Procedures Online ( IF 6.4 ) Pub Date : 2021-02-22 , DOI: 10.1186/s12575-021-00145-9
Fateme Khomari , Mohsen Nabi-Afjadi , Sahar Yarahmadi , Hanie Eskandari , Elham Bahreini

The proteostasis network includes all the factors that control the function of proteins in their native state and minimize their non-functional or harmful reactions. The molecular chaperones, the important mediator in the proteostasis network can be considered as any protein that contributes to proper folding and assembly of other macromolecules, through maturating of unfolded or partially folded macromolecules, refolding of stress-denatured proteins, and modifying oligomeric assembly, otherwise it leads to their proteolytic degradation. Viruses that use the hosts’ gene expression tools and protein synthesis apparatus to survive and replicate, are obviously protected by such a host chaperone system. This means that many viruses use members of the hosts’ chaperoning system to infect the target cells, replicate, and spread. During viral infection, increase in endoplasmic reticulum (ER) stress due to high expression of viral proteins enhances the level of heat shock proteins (HSPs) and induces cell apoptosis or necrosis. Indeed, evidence suggests that ER stress and the induction of unfolded protein response (UPR) may be a major aspect of the corona-host virus interaction. In addition, several clinical reports have confirmed the autoimmune phenomena in COVID-19-patients, and a strong association between this autoimmunity and severe SARS-CoV-2 infection. Part of such autoimmunity is due to shared epitopes among the virus and host. This article reviews the proteostasis network and its relationship to the immune system in SARS-CoV-2 infection.

中文翻译:

细胞变形蛋白网络对SARS-CoV-2存活的影响

蛋白质稳态网络包括所有控制蛋白质天然状态功能并使非功能性或有害反应最小化的因素。分子伴侣(蛋白伴侣网络中的重要介体)可以被认为是通过未折叠或部分折叠的大分子的成熟,应力变性蛋白质的重折叠以及修饰寡聚体组装而有助于其他大分子正确折叠和组装的任何蛋白质。它导致它们的蛋白水解降解。使用宿主的基因表达工具和蛋白质合成仪器存活和复制的病毒显然受到这种宿主伴侣系统的保护。这意味着许多病毒使用宿主的陪伴系统成员感染目标细胞,进行复制和传播。在病毒感染期间 由于病毒蛋白的高表达导致内质网(ER)压力增加,从而提高了热休克蛋白(HSP)的水平,并诱导了细胞凋亡或坏死。确实,有证据表明,内质网应激和未折叠蛋白应答(UPR)的诱导可能是日冕-宿主病毒相互作用的主要方面。此外,一些临床报告已经证实了COVID-19患者的自身免疫现象,以及这种自身免疫与严重SARS-CoV-2感染之间的密切联系。这种自身免疫的一部​​分归因于病毒和宿主之间共有的表位。本文综述了SARS-CoV-2感染中的蛋白质稳态网络及其与免疫系统的关系。
更新日期:2021-02-23
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