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SARS-CoV-2 劫持宿主 CD55、CD59 和因子 H，从而削弱抗体依赖性补体介导的细胞溶解作用。

SARS-CoV-2 hijacks host CD55, CD59 and factor H to impair antibody-dependent complement-mediated lysis.

机构信息

Medical University of Vienna, Center for Pathophysiology, Infectiology and Immunology, Institute for Hygiene and Applied Immunology, Vienna, Austria.

Medical University of Innsbruck, Institute of Virology, Innsbruck, Austria.

出版信息

Emerg Microbes Infect. 2024 Dec;13(1):2417868. doi: 10.1080/22221751.2024.2417868. Epub 2024 Oct 28.

DOI:10.1080/22221751.2024.2417868
PMID:39435487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11520101/
Abstract

The complement system is a vital anti-microbial defence mechanism against circulating pathogens. Excessive complement activation can have deleterious outcomes for the host and is consequently tightly modulated by a set of membrane-associated and fluid-phase regulators of complement activation (RCAs). Here, we demonstrate that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks host cellular RCA members CD55 and CD59 and serum-derived Factor H (FH) to resist antibody-dependent complement-mediated lysis triggered by immunized human sera. Blockage of the biological functions of virion-associated CD55 and CD59 and competition of FH recruitment with functionally inactive recombinant FH-derived short consensus repeats SCR18-20 restore SARS-CoV-2 complement sensitivity in a synergistic manner. Moreover, complement-mediated virolysis is dependent on classical pathway activation and does not occur in the absence of virus-specific antibodies. Altogether, our findings present an intriguing immune escape mechanism that provides novel insights into the immunopathology observed in severe coronavirus disease 2019 (COVID-19).

摘要

补体系统是一种针对循环病原体的重要抗微生物防御机制。补体的过度激活会对宿主造成有害影响，因此，补体激活的一组膜相关和液相结合调节剂（RCAs）对其进行了严格的调节。在这里，我们证明严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）劫持宿主细胞 RCA 成员 CD55 和 CD59 以及血清来源的因子 H（FH），以抵抗由免疫人血清引发的抗体依赖性补体介导的裂解。阻断病毒相关 CD55 和 CD59 的生物学功能，以及用功能上无活性的重组 FH 衍生短补体反应重复序列 SCR18-20 竞争 FH 的募集，以协同方式恢复 SARS-CoV-2 的补体敏感性。此外，补体介导的病毒裂解依赖于经典途径的激活，并且在没有病毒特异性抗体的情况下不会发生。总之，我们的研究结果揭示了一种有趣的免疫逃逸机制，为严重冠状病毒病 2019（COVID-19）中观察到的免疫病理学提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/b7b70c7e9aa4/TEMI_A_2417868_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/512183913414/TEMI_A_2417868_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/97f14135574b/TEMI_A_2417868_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/97389cb34c28/TEMI_A_2417868_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/a36a93408370/TEMI_A_2417868_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/3a9b1fa5b413/TEMI_A_2417868_F0004_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/ae20683695fc/TEMI_A_2417868_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/b7b70c7e9aa4/TEMI_A_2417868_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/512183913414/TEMI_A_2417868_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/97f14135574b/TEMI_A_2417868_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/97389cb34c28/TEMI_A_2417868_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/a36a93408370/TEMI_A_2417868_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/3a9b1fa5b413/TEMI_A_2417868_F0004_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/ae20683695fc/TEMI_A_2417868_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/336e/11520101/b7b70c7e9aa4/TEMI_A_2417868_F0006_OC.jpg

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