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

X Ou, Y Liu, X Lei, P Li, D Mi, L Ren, L Guo… - Nature …, 2020 - nature.com
X Ou, Y Liu, X Lei, P Li, D Mi, L Ren, L Guo, R Guo, T Chen, J Hu, Z Xiang, Z Mu, X Chen…
Nature communications, 2020nature.com
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 …
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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