Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA.
Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA; Institute Pasteur & CNRS UMR 3569, Unité de Virologie Structurale, 75015, Paris, France.
Cell. 2019 Feb 21;176(5):1026-1039.e15. doi: 10.1016/j.cell.2018.12.028. Epub 2019 Jan 31.
Recent outbreaks of severe acute respiratory syndrome and Middle East respiratory syndrome, along with the threat of a future coronavirus-mediated pandemic, underscore the importance of finding ways to combat these viruses. The trimeric spike transmembrane glycoprotein S mediates entry into host cells and is the major target of neutralizing antibodies. To understand the humoral immune response elicited upon natural infections with coronaviruses, we structurally characterized the SARS-CoV and MERS-CoV S glycoproteins in complex with neutralizing antibodies isolated from human survivors. Although the two antibodies studied blocked attachment to the host cell receptor, only the anti-SARS-CoV S antibody triggered fusogenic conformational changes via receptor functional mimicry. These results provide a structural framework for understanding coronavirus neutralization by human antibodies and shed light on activation of coronavirus membrane fusion, which takes place through a receptor-driven ratcheting mechanism.
最近严重急性呼吸综合征和中东呼吸综合征的爆发,以及未来冠状病毒引发的大流行的威胁,突显了寻找对抗这些病毒方法的重要性。三聚体刺突跨膜糖蛋白 S 介导病毒进入宿主细胞,是中和抗体的主要靶标。为了了解冠状病毒自然感染引起的体液免疫反应,我们对从人类幸存者中分离出的中和抗体与 SARS-CoV 和 MERS-CoV S 糖蛋白复合物进行了结构表征。虽然研究中的两种抗体都能阻止与宿主细胞受体的附着,但只有抗 SARS-CoV S 抗体通过受体功能模拟触发了融合构象变化。这些结果为理解人类抗体对冠状病毒的中和作用提供了结构框架,并阐明了冠状病毒膜融合的激活机制,该机制通过受体驱动的棘轮机制发生。