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Structural and biochemical mechanism for increased infectivity and immune evasion of Omicron BA.2 variant compared to BA.1 and their possible mouse origins

Medicine and Health

Structural and biochemical mechanism for increased infectivity and immune evasion of Omicron BA.2 variant compared to BA.1 and their possible mouse origins

Y. Xu, C. Wu, et al.

Discover how the Omicron BA.2 variant outshines BA.1 in infectivity and immune evasion in groundbreaking research conducted by Youwei Xu, Canrong Wu, Xiaodan Cao, and their colleagues. This study uncovers the structural nuances of the spike trimer that enhance ACE2 binding, revealing potential evolutionary paths in coronavirus transmission among species.

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Playback language: English
Abstract
The Omicron BA.2 variant exhibits significantly higher infectivity and immune evasion compared to BA.1 and the wildtype strain. Structural analysis reveals that BA.2's spike trimer displays all three receptor-binding domains in an open conformation, facilitating ACE2 binding. While the therapeutic antibody JMB2002 effectively neutralizes both BA.1 and BA.2, the high binding affinity of both BA.1 and BA.2 spike trimers to mouse ACE2 suggests a potential evolutionary pathway involving a human-cat-mouse-human transmission cycle.
Publisher
Cell Research
Published On
May 31, 2022
Authors
Youwei Xu, Canrong Wu, Xiaodan Cao, Chunyin Gu, Heng Liu, Mengting Jiang, Xiaoxi Wang, Qingning Yuan, Kai Wu, Jia Liu, Deyi Wang, Xianqing He, Xueping Wang, Su-Jun Deng, H. Eric Xu, Wanchao Yin
Tags
Omicron BA.2
infectivity
immune evasion
spike trimer
ACE2 binding
therapeutic antibody
transmission cycle

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