Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV.
Identifieur interne : 000121 ( PubMed/Corpus ); précédent : 000120; suivant : 000122Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV.
Auteurs : 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 QianSource :
- Nature communications [ 2041-1723 ] ; 2020.
English descriptors
- KwdEn :
- Antibodies, Viral (immunology), Betacoronavirus (chemistry), Betacoronavirus (immunology), Betacoronavirus (physiology), Broadly Neutralizing Antibodies (immunology), Calcium Channels (metabolism), Cathepsin L (metabolism), Cathepsins (antagonists & inhibitors), Cathepsins (metabolism), Cell Fusion, Coronavirus Infections (immunology), Cross Reactions, Endocytosis, Giant Cells (physiology), HEK293 Cells, Humans, Neutralization Tests, Pandemics, Peptidyl-Dipeptidase A (metabolism), Phosphatidylinositol 3-Kinases (metabolism), Pneumonia, Viral (immunology), Protein Domains, Protein Multimerization, Receptors, Virus (metabolism), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Spike Glycoprotein, Coronavirus (chemistry), Spike Glycoprotein, Coronavirus (immunology), Spike Glycoprotein, Coronavirus (metabolism), Trypsin (metabolism), Virus Internalization.
- MESH :
- chemical , antagonists & inhibitors : Cathepsins.
- chemical , chemistry : Spike Glycoprotein, Coronavirus.
- chemical , immunology : Antibodies, Viral, Broadly Neutralizing Antibodies, Spike Glycoprotein, Coronavirus.
- chemistry : Betacoronavirus.
- immunology : Betacoronavirus, Coronavirus Infections, Pneumonia, Viral, SARS Virus, Severe Acute Respiratory Syndrome.
- chemical , metabolism : Calcium Channels, Cathepsin L, Cathepsins, Peptidyl-Dipeptidase A, Phosphatidylinositol 3-Kinases, Receptors, Virus, Spike Glycoprotein, Coronavirus, Trypsin.
- physiology : Betacoronavirus, Giant Cells.
- Cell Fusion, Cross Reactions, Endocytosis, HEK293 Cells, Humans, Neutralization Tests, Pandemics, Protein Domains, Protein Multimerization, Virus Internalization.
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.
DOI: 10.1038/s41467-020-15562-9
PubMed: 32221306
Links to Exploration step
pubmed:32221306Le document en format XML
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<term>Betacoronavirus (physiology)</term>
<term>Broadly Neutralizing Antibodies (immunology)</term>
<term>Calcium Channels (metabolism)</term>
<term>Cathepsin L (metabolism)</term>
<term>Cathepsins (antagonists & inhibitors)</term>
<term>Cathepsins (metabolism)</term>
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<term>Coronavirus Infections (immunology)</term>
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<term>Endocytosis</term>
<term>Giant Cells (physiology)</term>
<term>HEK293 Cells</term>
<term>Humans</term>
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<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
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<term>Protein Domains</term>
<term>Protein Multimerization</term>
<term>Receptors, Virus (metabolism)</term>
<term>SARS Virus (immunology)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Spike Glycoprotein, Coronavirus (chemistry)</term>
<term>Spike Glycoprotein, Coronavirus (immunology)</term>
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<term>Virus Internalization</term>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
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<DateCompleted><Year>2020</Year>
<Month>04</Month>
<Day>02</Day>
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<DateRevised><Year>2020</Year>
<Month>04</Month>
<Day>15</Day>
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<JournalIssue CitedMedium="Internet"><Volume>11</Volume>
<Issue>1</Issue>
<PubDate><Year>2020</Year>
<Month>03</Month>
<Day>27</Day>
</PubDate>
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<Title>Nature communications</Title>
<ISOAbbreviation>Nat Commun</ISOAbbreviation>
</Journal>
<ArticleTitle>Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV.</ArticleTitle>
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</Pagination>
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<Abstract><AbstractText>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.</AbstractText>
</Abstract>
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