Please use this identifier to cite or link to this item:
Data supporting figures, tables and supplementary information in the published article: Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV
Ou Xiuyuan.
Liu Yan.
Lei Xiaobo.
Li Pei.
Mi Dan.
Ren Lili.
Guo Li.
Guo Ruixuan.
Chen Ting.
Hu Jiaxin.
Xiang Zichun.
Mu Zhixia.
Chen Xing.
Chen Jieyong.
Hu Keping.
Jin Qi.
Wang Jianwei.
Qian Zhaohui.
Acceso Abierto
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.
Nature communications
Appears in Collections:Artículos científicos

Upload archives

File SizeFormat 
1107419.pdf2.09 MBAdobe PDFView/Open