SrasV1, PascalFrancis, Curation, bibRecord, 000480

Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection

Identifieur interne : 000480 ( PascalFrancis/Curation ); précédent : 000479; suivant : 000481

Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection

Auteurs : Vera S. F. Chan [Hong Kong] ; Kelvin Y. K. Chan [Hong Kong] ; YONGXIONG CHEN [Hong Kong] ; Leo L. M. Poon [Hong Kong] ; Annie N. Y. Cheung [Hong Kong] ; BOJIAN ZHENG [Hong Kong] ; Kwok-Hung Chan [Hong Kong] ; William Mak [Hong Kong] ; Hextan Y. S. Ngan [Hong Kong] ; XIAONING XU [Royaume-Uni] ; Gavin Screaton [Royaume-Uni] ; Paul K. H. Tam [Hong Kong] ; Jonathan M. Austyn [Royaume-Uni] ; Li-Chong Chan [Hong Kong] ; Shea-Ping Yip [Hong Kong] ; Malik Peiris [Hong Kong] ; Ui-Soon Khoo [Hong Kong] ; Chen-Lung S. Lin [Hong Kong]

Source :

Nature genetics [ 1061-4036 ] ; 2006.

RBID : Pascal:06-0214013

Descripteurs français

Pascal (Inist)
- Syndrome respiratoire aigu sévère, Coronavirus.

English descriptors

KwdEn :
- Coronavirus, Severe acute respiratory syndrome.

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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A02	`01`			`@0 NGENEC`
A03		`1`		`@0 Nat. genet.`
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A08	`01`	`1`	`ENG`	`@1 Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection`
A11	`01`	`1`		`@1 CHAN (Vera S. F.)`
A11	`02`	`1`		`@1 CHAN (Kelvin Y. K.)`
A11	`03`	`1`		`@1 YONGXIONG CHEN`
A11	`04`	`1`		`@1 POON (Leo L. M.)`
A11	`05`	`1`		`@1 CHEUNG (Annie N. Y.)`
A11	`06`	`1`		`@1 BOJIAN ZHENG`
A11	`07`	`1`		`@1 CHAN (Kwok-Hung)`
A11	`08`	`1`		`@1 MAK (William)`
A11	`09`	`1`		`@1 NGAN (Hextan Y. S.)`
A11	`10`	`1`		`@1 XIAONING XU`
A11	`11`	`1`		`@1 SCREATON (Gavin)`
A11	`12`	`1`		`@1 TAM (Paul K. H.)`
A11	`13`	`1`		`@1 AUSTYN (Jonathan M.)`
A11	`14`	`1`		`@1 CHAN (Li-Chong)`
A11	`15`	`1`		`@1 YIP (Shea-Ping)`
A11	`16`	`1`		`@1 PEIRIS (Malik)`
A11	`17`	`1`		`@1 KHOO (Ui-Soon)`
A11	`18`	`1`		`@1 LIN (Chen-Lung S.)`
A14	`01`			`@1 Department of Surgery, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road @3 HKG @Z 1 aut. @Z 3 aut. @Z 12 aut. @Z 18 aut.`
A14	`02`			`@1 Department of Pathology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road @3 HKG @Z 2 aut. @Z 5 aut. @Z 14 aut. @Z 17 aut.`
A14	`03`			`@1 Department of Obsterics and Gynecology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road @3 HKG @Z 2 aut. @Z 9 aut.`
A14	`04`			`@1 Department of Microbiology, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road @3 HKG @Z 4 aut. @Z 6 aut. @Z 7 aut. @Z 16 aut.`
A14	`05`			`@1 Department of Genome Research Centre, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road @3 HKG @Z 8 aut. @Z 12 aut.`
A14	`06`			`@1 Human Immunology Unit, The Weatherall Institute of Molecular Medicine, University of Oxford @2 Oxford @3 GBR @Z 10 aut.`
A14	`07`			`@1 Division of Medicine, Imperial College @2 London @3 GBR @Z 11 aut.`
A14	`08`			`@1 Nuffield Department of Surgery, University of Oxford @2 Oxford @3 GBR @Z 13 aut.`
A14	`09`			`@1 Department of Health Technology and Informatics, The Hong Kong Polytechnic University @3 HKG @Z 15 aut.`
A20				`@1 38-46`
A21				`@1 2006`
A23	`01`			`@0 ENG`
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A64	`01`	`1`		`@0 Nature genetics`
A66	`01`			`@0 GBR`
C01	`01`		`ENG`	@0 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.
C02	`01`	`X`		`@0 002A07`
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C03	`01`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 01`
C03	`02`	`X`	`FRE`	`@0 Coronavirus @2 NW @5 16`
C03	`02`	`X`	`ENG`	`@0 Coronavirus @2 NW @5 16`
C03	`02`	`X`	`SPA`	`@0 Coronavirus @2 NW @5 16`
C07	`01`	`X`	`FRE`	`@0 Virose`
C07	`01`	`X`	`ENG`	`@0 Viral disease`
C07	`01`	`X`	`SPA`	`@0 Virosis`
C07	`02`	`X`	`FRE`	`@0 Infection`
C07	`02`	`X`	`ENG`	`@0 Infection`
C07	`02`	`X`	`SPA`	`@0 Infección`
C07	`03`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`03`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
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C07	`04`	`X`	`FRE`	`@0 Nidovirales @2 NW`
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C07	`04`	`X`	`SPA`	`@0 Nidovirales @2 NW`
C07	`05`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`05`	`X`	`ENG`	`@0 Virus @2 NW`
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C07	`06`	`X`	`FRE`	`@0 Appareil respiratoire pathologie @5 19`
C07	`06`	`X`	`ENG`	`@0 Respiratory disease @5 19`
C07	`06`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 19`
C07	`07`	`X`	`FRE`	`@0 Poumon pathologie @5 20`
C07	`07`	`X`	`ENG`	`@0 Lung disease @5 20`
C07	`07`	`X`	`SPA`	`@0 Pulmón patología @5 20`
N21				`@1 135`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

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Le 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>
<affiliation wicri:level="1"><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>
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<author><name sortKey="Chan, Kelvin Y K" sort="Chan, Kelvin Y K" uniqKey="Chan K" first="Kelvin Y. K." last="Chan">Kelvin Y. K. Chan</name>
<affiliation wicri:level="1"><inist: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>
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<country>Hong Kong</country>
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<affiliation wicri:level="1"><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>
<s3>HKG</s3>
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<country>Hong Kong</country>
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</author>
<author><name sortKey="Yongxiong Chen" sort="Yongxiong Chen" uniqKey="Yongxiong Chen" last="Yongxiong Chen">YONGXIONG CHEN</name>
<affiliation wicri:level="1"><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>
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<author><name sortKey="Poon, Leo L M" sort="Poon, Leo L M" uniqKey="Poon L" first="Leo L. M." last="Poon">Leo L. M. Poon</name>
<affiliation wicri:level="1"><inist: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>
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</inist:fA14>
<country>Hong Kong</country>
</affiliation>
</author>
<author><name sortKey="Cheung, Annie N Y" sort="Cheung, Annie N Y" uniqKey="Cheung A" first="Annie N. Y." last="Cheung">Annie N. Y. Cheung</name>
<affiliation wicri:level="1"><inist: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>
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<country>Hong Kong</country>
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<author><name sortKey="Bojian Zheng" sort="Bojian Zheng" uniqKey="Bojian Zheng" last="Bojian Zheng">BOJIAN ZHENG</name>
<affiliation wicri:level="1"><inist: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>
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<author><name sortKey="Xiaoning Xu" sort="Xiaoning Xu" uniqKey="Xiaoning Xu" last="Xiaoning Xu">XIAONING XU</name>
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<affiliation wicri:level="1"><inist: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>
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<author><name sortKey="Chan, Li Chong" sort="Chan, Li Chong" uniqKey="Chan L" first="Li-Chong" last="Chan">Li-Chong Chan</name>
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</author>
<author><name sortKey="Yip, Shea Ping" sort="Yip, Shea Ping" uniqKey="Yip S" first="Shea-Ping" last="Yip">Shea-Ping Yip</name>
<affiliation wicri:level="1"><inist:fA14 i1="09"><s1>Department of Health Technology and Informatics, The Hong Kong Polytechnic University</s1>
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<country>Hong Kong</country>
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</author>
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<affiliation wicri:level="1"><inist: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>
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<country>Hong Kong</country>
</affiliation>
</author>
<author><name sortKey="Khoo, Ui Soon" sort="Khoo, Ui Soon" uniqKey="Khoo U" first="Ui-Soon" last="Khoo">Ui-Soon Khoo</name>
<affiliation wicri:level="1"><inist: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>
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<sZ>14 aut.</sZ>
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<country>Hong Kong</country>
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</author>
<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 wicri:level="1"><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>
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<sZ>3 aut.</sZ>
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<country>Hong Kong</country>
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<series><title level="j" type="main">Nature genetics</title>
<title level="j" type="abbreviated">Nat. genet.</title>
<idno type="ISSN">1061-4036</idno>
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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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<sZ>9 aut.</sZ>
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<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>
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<sZ>6 aut.</sZ>
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<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>
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Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection

Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection

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