Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection
Identifieur interne : 000510 ( PascalFrancis/Corpus ); précédent : 000509; suivant : 000511Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection
Auteurs : Vera S. F. Chan ; Kelvin Y. K. Chan ; YONGXIONG CHEN ; Leo L. M. Poon ; Annie N. Y. Cheung ; BOJIAN ZHENG ; Kwok-Hung Chan ; William Mak ; Hextan Y. S. Ngan ; XIAONING XU ; Gavin Screaton ; Paul K. H. Tam ; Jonathan M. Austyn ; Li-Chong Chan ; Shea-Ping Yip ; Malik Peiris ; Ui-Soon Khoo ; Chen-Lung S. LinSource :
- Nature genetics [ 1061-4036 ] ; 2006.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection.
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Format Inist (serveur)
NO : | PASCAL 06-0214013 INIST |
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ET : | Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection |
AU : | CHAN (Vera S. F.); CHAN (Kelvin Y. K.); YONGXIONG CHEN; POON (Leo L. M.); CHEUNG (Annie N. Y.); BOJIAN ZHENG; CHAN (Kwok-Hung); MAK (William); NGAN (Hextan Y. S.); XIAONING XU; SCREATON (Gavin); TAM (Paul K. H.); AUSTYN (Jonathan M.); CHAN (Li-Chong); YIP (Shea-Ping); PEIRIS (Malik); KHOO (Ui-Soon); LIN (Chen-Lung S.) |
AF : | Department of Surgery, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (1 aut., 3 aut., 12 aut., 18 aut.); Department of Pathology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (2 aut., 5 aut., 14 aut., 17 aut.); Department of Obsterics and Gynecology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (2 aut., 9 aut.); Department of Microbiology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (4 aut., 6 aut., 7 aut., 16 aut.); Department of Genome Research Centre, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (8 aut., 12 aut.); Human Immunology Unit, The Weatherall Institute of Molecular Medicine, University of Oxford/Oxford/Royaume-Uni (10 aut.); Division of Medicine, Imperial College/London/Royaume-Uni (11 aut.); Nuffield Department of Surgery, University of Oxford/Oxford/Royaume-Uni (13 aut.); Department of Health Technology and Informatics, The Hong Kong Polytechnic University/Hong-Kong (15 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Nature genetics; ISSN 1061-4036; Coden NGENEC; Royaume-Uni; Da. 2006; Vol. 38; No. 1; Pp. 38-46; Bibl. 49 ref. |
LA : | Anglais |
EA : | Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection. |
CC : | 002A07 |
FD : | Syndrome respiratoire aigu sévère; Coronavirus |
FG : | Virose; Infection; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie |
ED : | Severe acute respiratory syndrome; Coronavirus |
EG : | Viral disease; Infection; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease |
SD : | Síndrome respiratorio agudo severo; Coronavirus |
LO : | INIST-22883.354000153467120050 |
ID : | 06-0214013 |
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Pascal:06-0214013Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection</title>
<author><name sortKey="Chan, Vera S F" sort="Chan, Vera S F" uniqKey="Chan V" first="Vera S. F." last="Chan">Vera S. F. Chan</name>
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<affiliation><inist:fA14 i1="03"><s1>Department of Obsterics and Gynecology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road</s1>
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<author><name sortKey="Yongxiong Chen" sort="Yongxiong Chen" uniqKey="Yongxiong Chen" last="Yongxiong Chen">YONGXIONG CHEN</name>
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<author><name sortKey="Bojian Zheng" sort="Bojian Zheng" uniqKey="Bojian Zheng" last="Bojian Zheng">BOJIAN ZHENG</name>
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<author><name sortKey="Lin, Chen Lung S" sort="Lin, Chen Lung S" uniqKey="Lin C" first="Chen-Lung S." last="Lin">Chen-Lung S. Lin</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Surgery, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road</s1>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>18 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Nature genetics</title>
<title level="j" type="abbreviated">Nat. genet.</title>
<idno type="ISSN">1061-4036</idno>
<imprint><date when="2006">2006</date>
</imprint>
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<seriesStmt><title level="j" type="main">Nature genetics</title>
<title level="j" type="abbreviated">Nat. genet.</title>
<idno type="ISSN">1061-4036</idno>
</seriesStmt>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Coronavirus</term>
<term>Severe acute respiratory syndrome</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term>
<term>Coronavirus</term>
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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection.</div>
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<fA05><s2>38</s2>
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<fA08 i1="01" i2="1" l="ENG"><s1>Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection</s1>
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<fA11 i1="01" i2="1"><s1>CHAN (Vera S. F.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>CHAN (Kelvin Y. K.)</s1>
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<fA11 i1="03" i2="1"><s1>YONGXIONG CHEN</s1>
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<fA11 i1="06" i2="1"><s1>BOJIAN ZHENG</s1>
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<fA11 i1="08" i2="1"><s1>MAK (William)</s1>
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<fA11 i1="09" i2="1"><s1>NGAN (Hextan Y. S.)</s1>
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<fA11 i1="11" i2="1"><s1>SCREATON (Gavin)</s1>
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<fA11 i1="12" i2="1"><s1>TAM (Paul K. H.)</s1>
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<fA11 i1="13" i2="1"><s1>AUSTYN (Jonathan M.)</s1>
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<fA11 i1="14" i2="1"><s1>CHAN (Li-Chong)</s1>
</fA11>
<fA11 i1="15" i2="1"><s1>YIP (Shea-Ping)</s1>
</fA11>
<fA11 i1="16" i2="1"><s1>PEIRIS (Malik)</s1>
</fA11>
<fA11 i1="17" i2="1"><s1>KHOO (Ui-Soon)</s1>
</fA11>
<fA11 i1="18" i2="1"><s1>LIN (Chen-Lung S.)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Surgery, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road</s1>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>18 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Pathology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road</s1>
<s3>HKG</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>17 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Obsterics and Gynecology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road</s1>
<s3>HKG</s3>
<sZ>2 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Microbiology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road</s1>
<s3>HKG</s3>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>16 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Genome Research Centre, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road</s1>
<s3>HKG</s3>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Human Immunology Unit, The Weatherall Institute of Molecular Medicine, University of Oxford</s1>
<s2>Oxford</s2>
<s3>GBR</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Division of Medicine, Imperial College</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Nuffield Department of Surgery, University of Oxford</s1>
<s2>Oxford</s2>
<s3>GBR</s3>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>Department of Health Technology and Informatics, The Hong Kong Polytechnic University</s1>
<s3>HKG</s3>
<sZ>15 aut.</sZ>
</fA14>
<fA20><s1>38-46</s1>
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<fA21><s1>2006</s1>
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<s1>© 2006 INIST-CNRS. All rights reserved.</s1>
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<fA45><s0>49 ref.</s0>
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<fC01 i1="01" l="ENG"><s0>Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection.</s0>
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<fC03 i1="01" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
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</fC03>
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<s5>01</s5>
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<s5>16</s5>
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<s2>NW</s2>
<s5>16</s5>
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<fC03 i1="02" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>16</s5>
</fC03>
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<fC07 i1="01" i2="X" l="ENG"><s0>Viral disease</s0>
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<fC07 i1="01" i2="X" l="SPA"><s0>Virosis</s0>
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<s2>NW</s2>
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<fC07 i1="03" i2="X" l="SPA"><s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
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<s2>NW</s2>
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<fC07 i1="04" i2="X" l="ENG"><s0>Nidovirales</s0>
<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
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<s5>19</s5>
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<s5>19</s5>
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<s5>19</s5>
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<s5>20</s5>
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<fN21><s1>135</s1>
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<ET>Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection</ET>
<AU>CHAN (Vera S. F.); CHAN (Kelvin Y. K.); YONGXIONG CHEN; POON (Leo L. M.); CHEUNG (Annie N. Y.); BOJIAN ZHENG; CHAN (Kwok-Hung); MAK (William); NGAN (Hextan Y. S.); XIAONING XU; SCREATON (Gavin); TAM (Paul K. H.); AUSTYN (Jonathan M.); CHAN (Li-Chong); YIP (Shea-Ping); PEIRIS (Malik); KHOO (Ui-Soon); LIN (Chen-Lung S.)</AU>
<AF>Department of Surgery, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (1 aut., 3 aut., 12 aut., 18 aut.); Department of Pathology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (2 aut., 5 aut., 14 aut., 17 aut.); Department of Obsterics and Gynecology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (2 aut., 9 aut.); Department of Microbiology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (4 aut., 6 aut., 7 aut., 16 aut.); Department of Genome Research Centre, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road/Hong-Kong (8 aut., 12 aut.); Human Immunology Unit, The Weatherall Institute of Molecular Medicine, University of Oxford/Oxford/Royaume-Uni (10 aut.); Division of Medicine, Imperial College/London/Royaume-Uni (11 aut.); Nuffield Department of Surgery, University of Oxford/Oxford/Royaume-Uni (13 aut.); Department of Health Technology and Informatics, The Hong Kong Polytechnic University/Hong-Kong (15 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Nature genetics; ISSN 1061-4036; Coden NGENEC; Royaume-Uni; Da. 2006; Vol. 38; No. 1; Pp. 38-46; Bibl. 49 ref.</SO>
<LA>Anglais</LA>
<EA>Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection.</EA>
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<FG>Virose; Infection; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie</FG>
<ED>Severe acute respiratory syndrome; Coronavirus</ED>
<EG>Viral disease; Infection; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease</EG>
<SD>Síndrome respiratorio agudo severo; Coronavirus</SD>
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