Characterization of Spike Glycoprotein of SARS-CoV-2 on Virus Entry and Its Immune Cross-Reactivity With SARS-CoV

Xiuyuan Ou, Yan Liu, Xiaobo Lei, Pei Li, Dan Mi, Lili Ren, Li Guo, Ruixuan Guo, Ting Chen, Jiaxin Hu, Zichun Xiang, Zhixia Mu, Xing Chen, Jieyong Chen, Keping Hu, Qi Jin, Jianwei Wang, Zhaohui Qian

Nat Commun. 2020 Mar 27;11(1):1620.

PMID: 32221306

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP40312343	T62		40312-34-3	Price