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新冠病毒谱系 B.1.620 和 R.1 的宿主细胞进入和中和敏感性

Host Cell Entry and Neutralization Sensitivity of SARS-CoV-2 Lineages B.1.620 and R.1.

机构信息

Infection Biology Unit, German Primate Center, 37077 Göttingen, Germany.

Faculty of Biology and Psychology, Georg-August-University Göttingen, 37073 Göttingen, Germany.

出版信息

Viruses. 2022 Nov 9;14(11):2475. doi: 10.3390/v14112475.

Abstract

The spike (S) protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) facilitates viral entry into host cells and is the key target for neutralizing antibodies. The SARS-CoV-2 lineage B.1.620 carries fifteen mutations in the S protein and is spread in Africa, the US and Europe, while lineage R.1 harbors four mutations in S and infections were observed in several countries, particularly Japan and the US. However, the impact of the mutations in B.1.620 and R.1 S proteins on antibody-mediated neutralization and host cell entry are largely unknown. Here, we report that these mutations are compatible with robust ACE2 binding and entry into cell lines, and they markedly reduce neutralization by vaccine-induced antibodies. Our results reveal evasion of neutralizing antibodies by B.1.620 and R.1, which might have contributed to the spread of these lineages.

摘要

严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)的刺突(S)蛋白有助于病毒进入宿主细胞,是中和抗体的关键靶标。SARS-CoV-2 谱系 B.1.620 的 S 蛋白携带十五个突变,在非洲、美国和欧洲传播,而谱系 R.1 的 S 蛋白携带四个突变,在多个国家,特别是日本和美国观察到感染。然而,B.1.620 和 R.1 S 蛋白突变对抗体介导的中和作用和宿主细胞进入的影响在很大程度上是未知的。在这里,我们报告这些突变与 ACE2 结合和进入细胞系的强大能力兼容,并且它们显著降低了疫苗诱导的抗体的中和作用。我们的结果揭示了 B.1.620 和 R.1 对中和抗体的逃避,这可能导致了这些谱系的传播。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1690/9698971/d29483e86e3e/viruses-14-02475-g001.jpg

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