Department of Microbial Pathogenesis, Yale University, New Haven, CT, USA.
Center for Theoretical Biological Physics, Rice University, Houston, TX, USA.
Science. 2024 Aug 16;385(6710):757-765. doi: 10.1126/science.adn5658. Epub 2024 Aug 15.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein binds the receptor angiotensin converting enzyme 2 (ACE2) and drives virus-host membrane fusion through refolding of its S2 domain. Whereas the S1 domain contains high sequence variability, the S2 domain is conserved and is a promising pan-betacoronavirus vaccine target. We applied cryo-electron tomography to capture intermediates of S2 refolding and understand inhibition by antibodies to the S2 stem-helix. Subtomogram averaging revealed ACE2 dimers cross-linking spikes before transitioning into S2 intermediates, which were captured at various stages of refolding. Pan-betacoronavirus neutralizing antibodies targeting the S2 stem-helix bound to and inhibited refolding of spike prehairpin intermediates. Combined with molecular dynamics simulations, these structures elucidate the process of SARS-CoV-2 entry and reveal how pan-betacoronavirus S2-targeting antibodies neutralize infectivity by arresting prehairpin intermediates.
严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)的刺突蛋白与受体血管紧张素转化酶 2(ACE2)结合,并通过其 S2 结构域的重折叠驱动病毒-宿主膜融合。虽然 S1 结构域包含高度的序列变异性,但 S2 结构域是保守的,是一种有前途的泛β冠状病毒疫苗靶点。我们应用冷冻电镜断层扫描来捕获 S2 重折叠的中间体,并了解针对 S2 茎-螺旋的抗体的抑制作用。亚断层平均显示 ACE2 二聚体在转变为 S2 中间体之前交联刺突,这些中间体在重折叠的各个阶段被捕获。针对 S2 茎-螺旋的泛β冠状病毒中和抗体结合并抑制了发夹前中间体的重折叠。结合分子动力学模拟,这些结构阐明了 SARS-CoV-2 进入的过程,并揭示了泛β冠状病毒 S2 靶向抗体如何通过阻止发夹前中间体来中和感染力。