Structure-based evidence for the enhanced transmissibility of the dominant SARS-CoV-2 B.1.1.7 variant (Alpha)
Shuai Xia, Zuoling Wen, Lijue Wang, Qiaoshuai Lan, Fanke Jiao, Linhua Tai, Qian Wang, Fei Sun, Shibo Jiang, Lu Lu, Yun Zhu
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in over 245 million infections and ~5 million deaths, severely threatening global public health. Moreover, numerous SARS-CoV-2 variants of concern (VOCs) with even higher transmissibility, such as B.1.1.7 (Alpha), B.1.351 (Beta), B.1. 617.2 (Delta), and C.37 (Lambda), are continuously emerging 1 . Monitoring these dominant SARS-CoV-2 variants and exploring the potential reason for their higher transmissibility are important for controlling the current COVID-19 pandemic. B.1.1.7, the first SARS-CoV-2 VOC, was first identified on September 20, 2020 in the United Kingdom (UK) and quickly became the locally dominant circulating mutant. Currently, it has spread to more than 90 countries, causing ~10 million infections (https://covlineages.org/global_report.html). Previous studies have reported that the B.1.1.7 variant shows a significant increase in the effective reproductive rate with increased secondary attack rate 2 . However, basic studies elucidating the mechanism underlying the increased infectivity of the B.1.1.7 variant are lacking. In particular, structural studies of the complex containing the B.1.1.7 mutant spike (S) protein and hACE2 receptor are not currently available.