Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV

Xiuyuan Ou(Chinese Academy of Medical Sciences & Peking Union Medical College), Yan Liu(Chinese Academy of Medical Sciences & Peking Union Medical College), Xiaobo Lei(Chinese Academy of Medical Sciences & Peking Union Medical College), Pei Li(Chinese Academy of Medical Sciences & Peking Union Medical College), Dan Mi(Chinese Academy of Medical Sciences & Peking Union Medical College), Lili Ren(Chinese Academy of Medical Sciences & Peking Union Medical College), Li Guo(Chinese Academy of Medical Sciences & Peking Union Medical College), Ruixuan Guo(Chinese Academy of Medical Sciences & Peking Union Medical College), Ting Chen(Chinese Academy of Medical Sciences & Peking Union Medical College), Jiaxin Hu(Chinese Academy of Medical Sciences & Peking Union Medical College), Zichun Xiang(Chinese Academy of Medical Sciences & Peking Union Medical College), Zhixia Mu(Chinese Academy of Medical Sciences & Peking Union Medical College), Xing Chen(Chinese Academy of Medical Sciences & Peking Union Medical College), Jieyong Chen, Keping Hu(Chinese Academy of Medical Sciences & Peking Union Medical College), Qi Jin(Chinese Academy of Medical Sciences & Peking Union Medical College), Jianwei Wang(Chinese Academy of Medical Sciences & Peking Union Medical College), Zhaohui Qian(Chinese Academy of Medical Sciences & Peking Union Medical College)
Nature Communications
March 27, 2020
10.1038/s41467-020-15562-9
Cited by 3,406Open Access
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Abstract

Since 2002, beta coronaviruses (CoV) have caused three zoonotic outbreaks, SARS-CoV in 2002-2003, MERS-CoV in 2012, and the newly emerged SARS-CoV-2 in late 2019. However, little is currently known about the biology of SARS-CoV-2. Here, using SARS-CoV-2 S protein pseudovirus system, we confirm that human angiotensin converting enzyme 2 (hACE2) is the receptor for SARS-CoV-2, find that SARS-CoV-2 enters 293/hACE2 cells mainly through endocytosis, that PIKfyve, TPC2, and cathepsin L are critical for entry, and that SARS-CoV-2 S protein is less stable than SARS-CoV S. Polyclonal anti-SARS S1 antibodies T62 inhibit entry of SARS-CoV S but not SARS-CoV-2 S pseudovirions. Further studies using recovered SARS and COVID-19 patients' sera show limited cross-neutralization, suggesting that recovery from one infection might not protect against the other. Our results present potential targets for development of drugs and vaccines for SARS-CoV-2.

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