Omicron Variant (B.1.1.529): Infectivity, Vaccine Breakthrough, and Antibody Resistance

被引:313
|
作者
Chen, Jiahui [1 ]
Wang, Rui [1 ]
Gilby, Nancy Benovich [2 ]
Wei, Guo-Wei [1 ,3 ,4 ]
机构
[1] Michigan State Univ, Dept Math, E Lansing, MI 48824 USA
[2] Spartan Innovat, E Lansing, MI 48823 USA
[3] Michigan State Univ, Dept Elect & Comp Engn, E Lansing, MI 48824 USA
[4] Michigan State Univ, Dept Biochem & Mol Biol, E Lansing, MI 48824 USA
关键词
RESPIRATORY-SYNDROME-CORONAVIRUS; MUTATIONS; PROTEIN; ESCAPE; ACE2;
D O I
10.1021/acs.jcim.1c01451
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
The latest severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variant Omicron (B.1.1.529) has ushered panic responses around the world due to its contagious and vaccine escape mutations. The essential infectivity and antibody resistance of the SARS-CoV-2 variant are determined by its mutations on the spike (S) protein receptor-binding domain (RBD). However, a complete experimental evaluation of Omicron might take weeks or even months. Here, we present a comprehensive quantitative analysis of Omicron's infectivity, vaccine breakthrough, and antibody resistance. An artificial intelligence (AI) model, which has been trained with tens of thousands of experimental data and extensively validated by experimental results on SARS-CoV-2, reveals that Omicron may be over 10 times more contagious than the original virus or about 2.8 times as infectious as the Delta variant. On the basis of 185 three-dimensional (3D) structures of antibody-RBD complexes, we unveil that Omicron may have an 88% likelihood to escape current vaccines. The U.S. Food and Drug Administration (FDA)-approved monoclonal antibodies (mAbs) from Eli Lilly may be seriously compromised. Omicron may also diminish the efficacy of mAbs from AstraZeneca, Regeneron mAb cocktail, Celltrion, and Rockefeller University. However, its impacts on GlaxoSmithKline's sotrovimab appear to be mild. Our work calls for new strategies to develop the next generation mutation-proof SARS-CoV-2 vaccines and antibodies.
引用
收藏
页码:412 / 422
页数:11
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