Bocquet-Garçon Annelise
Immunology, Independent Researcher, Béthune, FRA.
Cureus. 2024 Mar 26;16(3):e57008. doi: 10.7759/cureus.57008. eCollection 2024 Mar.
The Spike protein enables the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection by binding to multiple receptors, including the angiotensin-converting enzyme 2 (ACE2). Scientific studies also indicate that Spike is involved in severe forms of coronavirus disease 2019 (COVID-19), "long-haul COVID diseases" - also known as "long COVID syndromes" or "post-acute sequelae of SARS-CoV-2 infection" (PACS) - or, recently, in adverse reactions to lipid nanoparticle-messenger ribonucleic acid (mRNA) vaccines or other anti-COVID19 products. Numerous mutations, notably within the subunit 1 of Spike (S1), prevent neutralization by antibodies, but more generally, the virus has developed numerous strategies to avoid immune system surveillance, especially type-I interferons (IFN-I). Meanwhile, a "hyperinflammatory" state, named "cytokine storm," sets in. However, what role does the Spike protein play in the immune escape mechanisms? Can its inflammatory activities affect IFN-I? Does Spike block IFN-I or hijack them for the virus benefits? What are the other potential consequences? This article was written to provide an up-to-date and more general overview of the impact of the Spike protein on the innate immune system and its effectors at the molecular level.
刺突蛋白通过与包括血管紧张素转换酶2（ACE2）在内的多种受体结合，实现严重急性呼吸综合征冠状病毒2（SARS-CoV-2）的感染。科学研究还表明，刺突蛋白与2019冠状病毒病（COVID-19）的严重形式、“长期新冠疾病”（也称为“长新冠综合征”或“SARS-CoV-2感染的急性后遗症”（PACS））有关，或者最近与脂质纳米颗粒信使核糖核酸（mRNA）疫苗或其他抗COVID-19产品的不良反应有关。许多突变，尤其是在刺突蛋白亚基1（S1）内的突变，可阻止抗体的中和作用，但更普遍的是，病毒已经发展出多种策略来逃避免疫系统的监测，尤其是I型干扰素（IFN-I）。与此同时，一种名为“细胞因子风暴”的“过度炎症”状态开始出现。然而，刺突蛋白在免疫逃逸机制中起什么作用？其炎症活性会影响IFN-I吗？刺突蛋白是阻断IFN-I还是劫持它们以利于病毒？还有哪些其他潜在后果？撰写本文的目的是提供关于刺突蛋白对先天免疫系统及其效应分子在分子水平上影响的最新且更全面的概述。
