Identification of Common Deletions in the Spike Protein of Severe Acute Respiratory Syndrome Coronavirus 2
Zhe Liu, Huanying Zheng, Huifang Lin, Mingyue Li, Runyu Yuan, Jinju Peng, Qianling Xiong, Jiufeng Sun, Baisheng Li, Jie Wu, Lina Yi, Xiaofang Peng, Huan Zhang, Wei Zhang, Ruben J. G. Hulswit, Nick Loman, Andrew Rambaut, Changwen Ke, Thomas A. Bowden, Oliver G. Pybus, Jing Lu
Abstract
The spike protein determines the infectivity and host range of coronaviruses. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has two unique features in its spike protein, the receptor binding domain and an insertion of 12 nucleotides at the S1/S2 boundary resulting in a furin-like cleavage site. Here, we identified two deletion variants of SARS-CoV-2 that either directly affect the furin-like cleavage site itself (NSPRRAR) or a flanking sequence (QTQTN), and we investigated these deletions in cell isolates and clinical samples. The absence of the polybasic cleavage site in SARS-CoV-2 did not affect virus replication in Vero or Vero-E6 cells. Our data indicate the PRRAR sequence and the flanking QTQTN sequence are not fixed in vitro; thus, there appears to be distinct selection pressures on SARS-CoV-2 sequences in vitro and in vivo . Further investigation of the mechanism of generating these deletion variants and their infectivity in different animal models would improve our understanding of the origin and evolution of this virus.