Difference in Receptor Usage between Severe Acute Respiratory Syndrome (SARS) Coronavirus and SARS-Like Coronavirus of Bat Origin
Identifieur interne : 003507 ( Main/Exploration ); précédent : 003506; suivant : 003508Difference in Receptor Usage between Severe Acute Respiratory Syndrome (SARS) Coronavirus and SARS-Like Coronavirus of Bat Origin
Auteurs : WUZE REN [République populaire de Chine] ; XIUXIA QU [République populaire de Chine] ; WENDONG LI [République populaire de Chine] ; ZHENGGANG HAN [République populaire de Chine] ; MENG YU [Australie] ; PENG ZHOU [République populaire de Chine] ; Shu-Yi Zhang [République populaire de Chine] ; Lin-Fa Wang [Australie] ; HONGKUI DENG [République populaire de Chine] ; ZHENGLI SHI [République populaire de Chine]Source :
- Journal of virology [ 0022-538X ] ; 2008.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Severe acute respiratory syndrome (SARS) is caused by the SARS-associated coronavirus (SARS-CoV), which uses angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entry. A group of SARS-like CoVs (SL-CoVs) has been identified in horseshoe bats. SL-CoVs and SARS-CoVs share identical genome organizations and high sequence identities, with the main exception of the N terminus of the spike protein (S), known to be responsible for receptor binding in CoVs. In this study, we investigated the receptor usage of the SL-CoV S by combining a human immunodeficiency virus-based pseudovirus system with cell lines expressing the ACE2 molecules of human, civet, or horseshoe bat. In addition to full-length S of SL-CoV and SARS-CoV, a series of S chimeras was constructed by inserting different sequences of the SARS-CoV S into the SL-CoV S backbone. Several important observations were made from this study. First, the SL-CoV S was unable to use any of the three ACE2 molecules as its receptor. Second, the SARS-CoV S failed to enter cells expressing the bat ACE2. Third, the chimeric S covering the previously defined receptor-binding domain gained its ability to enter cells via human ACE2, albeit with different efficiencies for different constructs. Fourth, a minimal insert region (amino acids 310 to 518) was found to be sufficient to convert the SL-CoV S from non-ACE2 binding to human ACE2 binding, indicating that the SL-CoV S is largely compatible with SARS-CoV S protein both in structure and in function. The significance of these findings in relation to virus origin, virus recombination, and host switching is discussed.
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Shi" last="Zhengli Shi">ZHENGLI SHI</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences</s1><s2>Wuhan</s2><s3>CHN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>République populaire de Chine</country><placeName><settlement type="city">Wuhan</settlement><region type="région">Hubei</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">08-0181007</idno><date when="2008">2008</date><idno type="stanalyst">PASCAL 08-0181007 INIST</idno><idno type="RBID">Pascal:08-0181007</idno><idno type="wicri:Area/PascalFrancis/Corpus">000303</idno><idno type="wicri:Area/PascalFrancis/Curation">000685</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000287</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000287</idno><idno 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sortKey="Xiuxia Qu" sort="Xiuxia Qu" uniqKey="Xiuxia Qu" last="Xiuxia Qu">XIUXIA QU</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University</s1><s2>Beijing</s2><s3>CHN</s3><sZ>2 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>République populaire de Chine</country><placeName><settlement type="city">Pékin</settlement></placeName><orgName type="university">Université de Pékin</orgName></affiliation></author><author><name sortKey="Wendong Li" sort="Wendong Li" uniqKey="Wendong Li" last="Wendong Li">WENDONG LI</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences</s1><s2>Wuhan</s2><s3>CHN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>République populaire de Chine</country><placeName><settlement type="city">Wuhan</settlement><region type="région">Hubei</region></placeName></affiliation></author><author><name sortKey="Zhenggang Han" sort="Zhenggang Han" uniqKey="Zhenggang Han" last="Zhenggang Han">ZHENGGANG HAN</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences</s1><s2>Wuhan</s2><s3>CHN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>République populaire de Chine</country><placeName><settlement type="city">Wuhan</settlement><region type="région">Hubei</region></placeName></affiliation></author><author><name sortKey="Meng Yu" sort="Meng Yu" uniqKey="Meng Yu" last="Meng Yu">MENG YU</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>CSIRO Livestock Industries, Australian Animal Health Laboratory and Australian Biosecurity Cooperative Research Center for Emerging Infectious Diseases</s1><s2>Geelong</s2><s3>AUS</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Geelong</wicri:noRegion></affiliation></author><author><name sortKey="Peng Zhou" sort="Peng Zhou" uniqKey="Peng Zhou" last="Peng Zhou">PENG ZHOU</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences</s1><s2>Wuhan</s2><s3>CHN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>République populaire de Chine</country><placeName><settlement type="city">Wuhan</settlement><region type="région">Hubei</region></placeName></affiliation></author><author><name sortKey="Zhang, Shu Yi" sort="Zhang, Shu Yi" uniqKey="Zhang S" first="Shu-Yi" last="Zhang">Shu-Yi Zhang</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>School of Life Science, East China Normal University</s1><s2>Shanghai</s2><s3>CHN</s3><sZ>7 aut.</sZ></inist:fA14><country>République populaire de Chine</country><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Lin Fa" sort="Wang, Lin Fa" uniqKey="Wang L" first="Lin-Fa" last="Wang">Lin-Fa Wang</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>CSIRO Livestock Industries, Australian Animal Health Laboratory and Australian Biosecurity Cooperative Research Center for Emerging Infectious Diseases</s1><s2>Geelong</s2><s3>AUS</s3><sZ>5 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Geelong</wicri:noRegion></affiliation></author><author><name sortKey="Hongkui Deng" sort="Hongkui Deng" uniqKey="Hongkui Deng" last="Hongkui Deng">HONGKUI DENG</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University</s1><s2>Beijing</s2><s3>CHN</s3><sZ>2 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>République populaire de Chine</country><placeName><settlement type="city">Pékin</settlement></placeName><orgName type="university">Université de Pékin</orgName></affiliation></author><author><name sortKey="Zhengli Shi" sort="Zhengli Shi" uniqKey="Zhengli Shi" last="Zhengli Shi">ZHENGLI SHI</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences</s1><s2>Wuhan</s2><s3>CHN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>République populaire de Chine</country><placeName><settlement type="city">Wuhan</settlement><region type="région">Hubei</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of virology</title><title level="j" type="abbreviated">J. virol.</title><idno type="ISSN">0022-538X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute</term><term>Biological receptor</term><term>Origin</term><term>Severe acute respiratory syndrome virus</term><term>Virology</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Virus syndrome respiratoire aigu sévère</term><term>Récepteur biologique</term><term>Aigu</term><term>Origine</term><term>Virologie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is caused by the SARS-associated coronavirus (SARS-CoV), which uses angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entry. A group of SARS-like CoVs (SL-CoVs) has been identified in horseshoe bats. SL-CoVs and SARS-CoVs share identical genome organizations and high sequence identities, with the main exception of the N terminus of the spike protein (S), known to be responsible for receptor binding in CoVs. In this study, we investigated the receptor usage of the SL-CoV S by combining a human immunodeficiency virus-based pseudovirus system with cell lines expressing the ACE2 molecules of human, civet, or horseshoe bat. In addition to full-length S of SL-CoV and SARS-CoV, a series of S chimeras was constructed by inserting different sequences of the SARS-CoV S into the SL-CoV S backbone. Several important observations were made from this study. First, the SL-CoV S was unable to use any of the three ACE2 molecules as its receptor. Second, the SARS-CoV S failed to enter cells expressing the bat ACE2. Third, the chimeric S covering the previously defined receptor-binding domain gained its ability to enter cells via human ACE2, albeit with different efficiencies for different constructs. Fourth, a minimal insert region (amino acids 310 to 518) was found to be sufficient to convert the SL-CoV S from non-ACE2 binding to human ACE2 binding, indicating that the SL-CoV S is largely compatible with SARS-CoV S protein both in structure and in function. The significance of these findings in relation to virus origin, virus recombination, and host switching is discussed.</div></front></TEI><affiliations><list><country><li>Australie</li><li>République populaire de Chine</li></country><region><li>Hubei</li></region><settlement><li>Pékin</li><li>Wuhan</li></settlement><orgName><li>Université de Pékin</li></orgName></list><tree><country name="République populaire de Chine"><region name="Hubei"><name sortKey="Wuze Ren" sort="Wuze Ren" uniqKey="Wuze Ren" last="Wuze Ren">WUZE REN</name></region><name sortKey="Hongkui Deng" sort="Hongkui Deng" uniqKey="Hongkui Deng" last="Hongkui Deng">HONGKUI DENG</name><name sortKey="Peng Zhou" sort="Peng Zhou" uniqKey="Peng Zhou" last="Peng Zhou">PENG ZHOU</name><name sortKey="Wendong Li" sort="Wendong Li" uniqKey="Wendong Li" last="Wendong Li">WENDONG LI</name><name sortKey="Xiuxia Qu" sort="Xiuxia Qu" uniqKey="Xiuxia Qu" last="Xiuxia Qu">XIUXIA QU</name><name sortKey="Zhang, Shu Yi" sort="Zhang, Shu Yi" uniqKey="Zhang S" first="Shu-Yi" last="Zhang">Shu-Yi Zhang</name><name sortKey="Zhenggang Han" sort="Zhenggang Han" uniqKey="Zhenggang Han" last="Zhenggang Han">ZHENGGANG HAN</name><name sortKey="Zhengli Shi" sort="Zhengli Shi" uniqKey="Zhengli Shi" last="Zhengli Shi">ZHENGLI SHI</name></country><country name="Australie"><noRegion><name sortKey="Meng Yu" sort="Meng Yu" uniqKey="Meng Yu" last="Meng Yu">MENG YU</name></noRegion><name sortKey="Wang, Lin Fa" sort="Wang, Lin Fa" uniqKey="Wang L" first="Lin-Fa" last="Wang">Lin-Fa Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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