Receptor and viral determinants of SARS‐coronavirus adaptation to human ACE2
Identifieur interne : 000293 ( Istex/Curation ); précédent : 000292; suivant : 000294Receptor and viral determinants of SARS‐coronavirus adaptation to human ACE2
Auteurs : Wenhui Li [États-Unis] ; Chengsheng Zhang [Canada, République populaire de Chine] ; Jianhua Sui [États-Unis] ; Jens H. Kuhn [États-Unis, Allemagne] ; Michael J. Moore [États-Unis] ; Shiwen Luo [République populaire de Chine] ; Swee-Kee Wong [États-Unis] ; I-Chueh Huang [États-Unis] ; Keming Xu [République populaire de Chine] ; Natalya Vasilieva [États-Unis] ; Akikazu Murakami [États-Unis] ; Yaqing He [République populaire de Chine] ; Wayne A. Marasco [États-Unis] ; Yi Guan [République populaire de Chine, Hong Kong] ; Hyeryun Choe [États-Unis, Hong Kong] ; Michael Farzan [États-Unis, Hong Kong]Source :
- The EMBO Journal [ 0261-4189 ] ; 2005-04-20.
English descriptors
- Teeft :
- Accession number, Ace2, Ace2 variants, Asparagine, Biology organization, Biology organization adaptation, Cells transfected, Chimera, Civet, Civet ace2, Collectrin, Collectrin domain, Coronavirus, Cytometry, Embo, Embo journal, Encoding, Farzan, Functional receptor, Glycoprotein, Guan, Human ace2, Liang, Lysine, Murine, Outbreak, Palm civet, Palm civets, Plasmid, Plasmid encoding, Plasmids encoding, Pseudotyped, Rbds, Receptor, Residue, Respiratory syndrome, Respiratory syndrome coronavirus, Sars, Sars coronavirus, Syndrome, Threonine, Tor2, Transfected, Variant, Virol, Wang, Wong, Zhang, Zheng.
Abstract
Human angiotensin‐converting enzyme 2 (ACE2) is a functional receptor for SARS coronavirus (SARS‐CoV). Here we identify the SARS‐CoV spike (S)‐protein‐binding site on ACE2. We also compare S proteins of SARS‐CoV isolated during the 2002–2003 SARS outbreak and during the much less severe 2003–2004 outbreak, and from palm civets, a possible source of SARS‐CoV found in humans. All three S proteins bound to and utilized palm‐civet ACE2 efficiently, but the latter two S proteins utilized human ACE2 markedly less efficiently than did the S protein obtained during the earlier human outbreak. The lower affinity of these S proteins could be complemented by altering specific residues within the S‐protein‐binding site of human ACE2 to those of civet ACE2, or by altering S‐protein residues 479 and 487 to residues conserved during the 2002–2003 outbreak. Collectively, these data describe molecular interactions important to the adaptation of SARS‐CoV to human cells, and provide insight into the severity of the 2002–2003 SARS epidemic.
Url:
DOI: 10.1038/sj.emboj.7600640
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Kuhn</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, Southborough, MA, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, Southborough, MA</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Department of Biology, Chemistry, Pharmacy, Freie Universität Berlin, Berlin, Germany</mods:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Biology, Chemistry, Pharmacy, Freie Universität Berlin, Berlin</wicri:regionArea></affiliation></author><author><name sortKey="Moore, Michael J" sort="Moore, Michael J" uniqKey="Moore M" first="Michael J" last="Moore">Michael J. Moore</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, MA, Southborough, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, MA, Southborough</wicri:regionArea></affiliation></author><author><name sortKey="Luo, Shiwen" sort="Luo, Shiwen" uniqKey="Luo S" first="Shiwen" last="Luo">Shiwen Luo</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, PRC</mods:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR</wicri:regionArea></affiliation></author><author><name sortKey="Wong, Swee Ee" sort="Wong, Swee Ee" uniqKey="Wong S" first="Swee-Kee" last="Wong">Swee-Kee Wong</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, MA, Southborough, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, MA, Southborough</wicri:regionArea></affiliation></author><author><name sortKey="Huang, I Hueh" sort="Huang, I Hueh" uniqKey="Huang I" first="I-Chueh" last="Huang">I-Chueh Huang</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, MA, Southborough, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, MA, Southborough</wicri:regionArea></affiliation></author><author><name sortKey="Xu, Keming" sort="Xu, Keming" uniqKey="Xu K" first="Keming" last="Xu">Keming Xu</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, PRC</mods:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR</wicri:regionArea></affiliation></author><author><name sortKey="Vasilieva, Natalya" sort="Vasilieva, Natalya" uniqKey="Vasilieva N" first="Natalya" last="Vasilieva">Natalya Vasilieva</name><affiliation wicri:level="1"><mods:affiliation>Department of Pediatrics, Children's Hospital, Harvard Medical School, MA, Boston, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics, Children's Hospital, Harvard Medical School, MA, Boston</wicri:regionArea></affiliation></author><author><name sortKey="Murakami, Akikazu" sort="Murakami, Akikazu" uniqKey="Murakami A" first="Akikazu" last="Murakami">Akikazu Murakami</name><affiliation wicri:level="1"><mods:affiliation>Department of Medicine, Dana‐Farber Cancer Institute, Harvard Medical School, MA, Boston, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Dana‐Farber Cancer Institute, Harvard Medical School, MA, Boston</wicri:regionArea></affiliation></author><author><name sortKey="He, Yaqing" sort="He, Yaqing" uniqKey="He Y" first="Yaqing" last="He">Yaqing He</name><affiliation wicri:level="1"><mods:affiliation>Center for Disease Control and Prevention of Shenzhen, Guangdong Province, Shenzhen, PRC</mods:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Center for Disease Control and Prevention of Shenzhen, Guangdong Province, Shenzhen</wicri:regionArea></affiliation></author><author><name sortKey="Marasco, Wayne A" sort="Marasco, Wayne A" uniqKey="Marasco W" first="Wayne A" last="Marasco">Wayne A. Marasco</name><affiliation wicri:level="1"><mods:affiliation>Department of Medicine, Dana‐Farber Cancer Institute, Harvard Medical School, MA, Boston, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Dana‐Farber Cancer Institute, Harvard Medical School, MA, Boston</wicri:regionArea></affiliation></author><author><name sortKey="Guan, Yi" sort="Guan, Yi" uniqKey="Guan Y" first="Yi" last="Guan">Yi Guan</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, PRC</mods:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: yguan@hkucc.hku.hk</mods:affiliation><country wicri:rule="url">Hong Kong</country></affiliation></author><author><name sortKey="Choe, Hyeryun" sort="Choe, Hyeryun" uniqKey="Choe H" first="Hyeryun" last="Choe">Hyeryun Choe</name><affiliation wicri:level="1"><mods:affiliation>Department of Pediatrics, Children's Hospital, Harvard Medical School, MA, Boston, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics, Children's Hospital, Harvard Medical School, MA, Boston</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: yguan@hkucc.hku.hk</mods:affiliation><country wicri:rule="url">Hong Kong</country></affiliation></author><author><name sortKey="Farzan, Michael" sort="Farzan, Michael" uniqKey="Farzan M" first="Michael" last="Farzan">Michael Farzan</name><affiliation wicri:level="1"><mods:affiliation>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, MA, Southborough, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, MA, Southborough</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: yguan@hkucc.hku.hk</mods:affiliation><country wicri:rule="url">Hong Kong</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">The EMBO Journal</title><title level="j" type="alt">THE EMBO JOURNAL</title><idno type="ISSN">0261-4189</idno><idno type="eISSN">1460-2075</idno><imprint><biblScope unit="vol">24</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1634">1634</biblScope><biblScope unit="page" to="1643">1643</biblScope><biblScope unit="page-count">10</biblScope><publisher>John Wiley & Sons, Ltd</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2005-04-20">2005-04-20</date></imprint><idno type="ISSN">0261-4189</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0261-4189</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Accession number</term><term>Ace2</term><term>Ace2 variants</term><term>Asparagine</term><term>Biology organization</term><term>Biology organization adaptation</term><term>Cells transfected</term><term>Chimera</term><term>Civet</term><term>Civet ace2</term><term>Collectrin</term><term>Collectrin domain</term><term>Coronavirus</term><term>Cytometry</term><term>Embo</term><term>Embo journal</term><term>Encoding</term><term>Farzan</term><term>Functional receptor</term><term>Glycoprotein</term><term>Guan</term><term>Human ace2</term><term>Liang</term><term>Lysine</term><term>Murine</term><term>Outbreak</term><term>Palm civet</term><term>Palm civets</term><term>Plasmid</term><term>Plasmid encoding</term><term>Plasmids encoding</term><term>Pseudotyped</term><term>Rbds</term><term>Receptor</term><term>Residue</term><term>Respiratory syndrome</term><term>Respiratory syndrome coronavirus</term><term>Sars</term><term>Sars coronavirus</term><term>Syndrome</term><term>Threonine</term><term>Tor2</term><term>Transfected</term><term>Variant</term><term>Virol</term><term>Wang</term><term>Wong</term><term>Zhang</term><term>Zheng</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Human angiotensin‐converting enzyme 2 (ACE2) is a functional receptor for SARS coronavirus (SARS‐CoV). Here we identify the SARS‐CoV spike (S)‐protein‐binding site on ACE2. We also compare S proteins of SARS‐CoV isolated during the 2002–2003 SARS outbreak and during the much less severe 2003–2004 outbreak, and from palm civets, a possible source of SARS‐CoV found in humans. All three S proteins bound to and utilized palm‐civet ACE2 efficiently, but the latter two S proteins utilized human ACE2 markedly less efficiently than did the S protein obtained during the earlier human outbreak. The lower affinity of these S proteins could be complemented by altering specific residues within the S‐protein‐binding site of human ACE2 to those of civet ACE2, or by altering S‐protein residues 479 and 487 to residues conserved during the 2002–2003 outbreak. Collectively, these data describe molecular interactions important to the adaptation of SARS‐CoV to human cells, and provide insight into the severity of the 2002–2003 SARS epidemic.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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