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从进化角度看,严重急性呼吸综合征冠状病毒2(SARS-CoV-2)逃避天然免疫系统的策略

Strategies Used by SARS-CoV-2 to Evade the Innate Immune System in an Evolutionary Perspective.

作者信息

Fan Hong, Tian Mingfu, Liu Siyu, Ye Chenglin, Li Zhiqiang, Wu Kailang, Zhu Chengliang

机构信息

Department of Clinical Laboratory, Institute of Translational Medicine, Renmin Hospital of Wuhan University, Wuhan 430060, China.

State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China.

出版信息

Pathogens. 2024 Dec 17;13(12):1117. doi: 10.3390/pathogens13121117.

DOI:10.3390/pathogens13121117
PMID:39770376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11677916/
Abstract

By the end of 2019, the COVID-19 pandemic, resulting from the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), had diffused widely across the globe, with 770 million infected individuals and over 7 million deaths reported. In addition to its high infectivity and pathogenicity and its rapid mutation rate, the unique capacity of SARS-CoV-2 to circumvent the immune system has also contributed to the widespread nature of this pandemic. SARS-CoV-2 elicits the onset of innate immune system activation and initiates antiviral responses once it has infected the host. While battling the host's immune responses, SARS-CoV-2 has established many countermeasures to evade attack and clearance. As the exploration of SARS-CoV-2 continues, substantial evidence has revealed that the 29 proteins synthesized by the SARS-CoV-2 genome are integral to the viral infection process. They not only facilitate viral replication and transmission, but also assist SARS-CoV-2 in escaping the host's immune defenses, positioning them as promising therapeutic targets that have attracted considerable attention in recent studies. This review summarizes the manner in which SARS-CoV-2 interfaces with the innate immune system, with a particular focus on the continuous evolution of SARS-CoV-2 and the implications of mutations.

摘要

截至2019年底,由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引发的新冠疫情已在全球广泛传播,报告的感染人数达7.7亿,死亡人数超过700万。除了具有高传染性、高致病性以及快速突变率外,SARS-CoV-2规避免疫系统的独特能力也促使了这场疫情的广泛传播。SARS-CoV-2一旦感染宿主,就会引发先天性免疫系统激活并启动抗病毒反应。在对抗宿主免疫反应的同时,SARS-CoV-2也建立了许多应对措施来逃避攻击和清除。随着对SARS-CoV-2研究的不断深入,大量证据表明,SARS-CoV-2基因组合成的29种蛋白质对于病毒感染过程至关重要。它们不仅促进病毒复制和传播,还帮助SARS-CoV-2逃避宿主的免疫防御,使其成为近年来研究中备受关注的有前景的治疗靶点。本综述总结了SARS-CoV-2与先天性免疫系统相互作用的方式,特别关注SARS-CoV-2的持续进化及其突变的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/942d/11677916/e2e3c0622550/pathogens-13-01117-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/942d/11677916/660de5419e24/pathogens-13-01117-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/942d/11677916/f7fb37cffac9/pathogens-13-01117-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/942d/11677916/e2e3c0622550/pathogens-13-01117-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/942d/11677916/660de5419e24/pathogens-13-01117-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/942d/11677916/f7fb37cffac9/pathogens-13-01117-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/942d/11677916/e2e3c0622550/pathogens-13-01117-g003.jpg

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