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. SARS-CoV-2 has spread globally. Here, the authors characterize the entry pathway of SARS-CoV-2, show that the SARS-CoV-2 spike protein is less stable than that of SARS-CoV, and show limited cross-neutralization activities between SARS-CoV and SARS-CoV-2 sera.
【저자키워드】 antibodies, viral infection, SARS virus, Virus-host interactions, 【초록키워드】 COVID-19, SARS-CoV-2, Vaccine, antibody, SARS-CoV, Infection, drug, Spike protein, hACE2, Spread, Outbreaks, pseudovirus, sera, zoonotic, cross-neutralization, CoV, target, receptor, Critical, SARS-CoV-2 S protein, cathepsin L, enzyme, entry pathway, SARS-CoV-2 S, cross-neutralization activity, SARS-CoV S, beta coronavirus, Cell, pseudovirions, PROTECT, caused, inhibit, less, biology of SARS-CoV-2, MERS-CoV in 2012, T62, the SARS-CoV-2, 【제목키워드】 SARS-CoV-2, SARS-CoV, spike glycoprotein, immune, cross-reactivity, virus entry, characterization,