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SARS-CoV-2 核衣壳蛋白并非补体凝集素途径过度激活的原因。

SARS-CoV-2 Nucleocapsid Protein Is Not Responsible for Over-Activation of Complement Lectin Pathway.

机构信息

Institute of Molecular Life Sciences, HUN-REN Research Centre for Natural Sciences, Hungarian Research Network, H-1117 Budapest, Hungary.

Department of Organic Chemistry and Technology, Faculty of Chemical Technology and Biotechnology, Budapest University of Technology and Economics, H-1111 Budapest, Hungary.

出版信息

Int J Mol Sci. 2024 Jul 4;25(13):7343. doi: 10.3390/ijms25137343.

Abstract

The nucleocapsid (N) protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a viral structural protein that is abundant in the circulation of infected individuals. Previous published studies reported controversial data about the role of the N protein in the activation of the complement system. It was suggested that the N protein directly interacts with mannose-binding lectin-associated serine protease-2 (MASP-2) and stimulates lectin pathway overactivation/activity. In order to check these data and to reveal the mechanism of activation, we examined the effect of the N protein on lectin pathway activation. We found that the N protein does not bind to MASP-2 and MASP-1 and it does not stimulate lectin pathway activity in normal human serum. Furthermore, the N protein does not facilitate the activation of zymogen MASP-2, which is MASP-1 dependent. Moreover, the N protein does not boost the enzymatic activity of MASP-2 either on synthetic or on protein substrates. In some of our experiments, we observed that MASP-2 digests the N protein. However, it is questionable, whether this activity is biologically relevant. Although surface-bound N protein did not activate the lectin pathway, it did trigger the alternative pathway in 10% human serum. Additionally, we detected some classical pathway activation by the N protein. Nevertheless, we demonstrated that this activation was induced by the bound nucleic acid, rather than by the N protein itself.

摘要

严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)的核衣壳(N)蛋白是一种丰富存在于感染个体循环中的病毒结构蛋白。先前发表的研究报告了关于 N 蛋白在补体系统激活中的作用的有争议的数据。有人提出,N 蛋白直接与甘露糖结合凝集素相关丝氨酸蛋白酶-2(MASP-2)相互作用,并刺激凝集素途径过度激活/活性。为了检查这些数据并揭示激活机制,我们检查了 N 蛋白对凝集素途径激活的影响。我们发现 N 蛋白不与 MASP-2 和 MASP-1 结合,也不会刺激正常人血清中的凝集素途径活性。此外,N 蛋白不会促进依赖于 MASP-1 的酶原 MASP-2 的激活。此外,N 蛋白也不会增强 MASP-2 在合成或蛋白质底物上的酶活性。在我们的一些实验中,我们观察到 MASP-2 消化 N 蛋白。然而,这种活性是否具有生物学相关性是值得怀疑的。尽管表面结合的 N 蛋白不能激活凝集素途径,但它确实可以在 10%的人血清中触发替代途径。此外,我们还检测到 N 蛋白对经典途径的一些激活。然而,我们证明这种激活是由结合的核酸而非 N 蛋白本身诱导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c31d/11242754/d13ee15fd820/ijms-25-07343-g001.jpg

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