Tang Haijun, Gao Long, Wu Zhao, Meng Fang, Zhao Xin, Shao Yun, Hou Guocun, Du Xiaohong, Qin F Xiao-Feng
Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Suzhou Institute of Systems Medicine, Suzhou, China.
Front Immunol. 2022 Mar 16;13:836232. doi: 10.3389/fimmu.2022.836232. eCollection 2022.
The continuous emergence of SARS-coronavirus 2 (SARS-CoV-2) variants, especially the variants of concern (VOC), exacerbated the impact of the coronavirus disease 2019 (COVID-19) pandemic. As the key of viral entry into host cells, the spike (S) protein is the major target of therapeutic monoclonal antibodies (mAbs) and polyclonal antibodies elicited by infection or vaccination. However, the mutations of S protein in variants may change the infectivity and antigenicity of SARS-CoV-2, leading to the immune escape from those neutralizing antibodies. To characterize the mutations of S protein in newly emerging variants, the proteolytic property and binding affinity with receptor were assessed, and the vesicular stomatitis virus (VSV)-based pseudovirus system was used to assess the infectivity and immune escape. We found that some SARS-CoV-2 variants have changed significantly in viral infectivity; especially, B.1.617.2 is more likely to infect less susceptible cells than D614G, and the virus infection process can be completed in a shorter time. In addition, neutralizing mAbs and vaccinated sera partially or completely failed to inhibit host cell entry mediated by the S protein of certain SARS-CoV-2 variants. However, SARS-CoV-2 variant S protein-mediated viral infection can still be blocked by protease inhibitors and endocytosis inhibitors. This work provides a deeper understanding of the rise and evolution of SARS-CoV-2 variants and their immune evasion.
严重急性呼吸综合征冠状病毒2(SARS-CoV-2)变体不断出现,尤其是值得关注的变体(VOC),加剧了2019冠状病毒病(COVID-19)大流行的影响。作为病毒进入宿主细胞的关键,刺突(S)蛋白是治疗性单克隆抗体(mAb)以及感染或疫苗接种引发的多克隆抗体的主要靶点。然而,变体中S蛋白的突变可能会改变SARS-CoV-2的传染性和抗原性,导致这些中和抗体出现免疫逃逸。为了表征新出现变体中S蛋白的突变情况,评估了其蛋白水解特性和与受体的结合亲和力,并使用基于水泡性口炎病毒(VSV)的假病毒系统评估传染性和免疫逃逸。我们发现,一些SARS-CoV-2变体的病毒传染性发生了显著变化;特别是,B.1.617.2比D614G更易感染较难感染的细胞,且病毒感染过程可在更短时间内完成。此外,中和单克隆抗体和接种疫苗后的血清部分或完全无法抑制某些SARS-CoV-2变体的S蛋白介导的宿主细胞进入。然而,SARS-CoV-2变体S蛋白介导的病毒感染仍可被蛋白酶抑制剂和内吞作用抑制剂阻断。这项工作为深入了解SARS-CoV-2变体的出现、进化及其免疫逃逸提供了依据。