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dc.contributor.authorOu, Xiuyuan et al.
dc.date.accessioned2020-12-17T21:41:02Z
dc.date.available2020-12-17T21:41:02Z
dc.date.issued2020-03-27
dc.identifier.urihttps://doi.org/10.1038/s41467-020-15562-9en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12663/2422
dc.description.abstractSince 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.en_US
dc.languageEnglishen_US
dc.subjectCOVID-19en_US
dc.subjectCoronavirusen_US
dc.subjectCoronavirus Infectionsen_US
dc.subjectInfectious Diseasesen_US
dc.subjectAntibodiesen_US
dc.subjectSARS-CoV-2en_US
dc.subjectBetacoronavirusen_US
dc.subjectVirus Diseasesen_US
dc.subjectHost Microbial Interactionsen_US
dc.titleCharacterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoVen_US
eihealth.countryOthersen_US
eihealth.categoryVirus: natural history, transmission and diagnosticsen_US
eihealth.categoryCandidate therapeutics RDen_US
eihealth.typePublished Articleen_US
eihealth.maincategorySave Lives / Salvar Vidasen_US
dc.relation.ispartofjournalNature Communicationsen_US


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