SrasV1, PascalFrancis, Corpus, bibRecord, 000575

Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection

Identifieur interne : 000575 ( PascalFrancis/Corpus ); précédent : 000574; suivant : 000576

Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection

Auteurs : HONGXING ZHANG ; GANGQIAO ZHOU ; LIANTENG ZHI ; HAO YANG ; YUN ZHAI ; XIAOJIA DONG ; XIUMEI ZHANG ; XUE GAO ; YUNPING ZHU ; FUCHU HE

Source :

The Journal of infectious diseases [ 0022-1899 ] ; 2005.

RBID : Pascal:05-0492671

Descripteurs français

Pascal (Inist)
- Coronavirus, Mannose, Lectine, Polymorphisme, Microbiologie, Infection, Syndrome respiratoire aigu sévère, Association genetique.

English descriptors

KwdEn :
- Coronavirus, Infection, Lectin, Mannose, Microbiology, Polymorphism, Severe acute respiratory syndrome.

Abstract

Background. Genetic determinants of susceptibility to severe acute respiratory syndrome coronavirus (SARS-CoV) infection remain unknown. We assessed whether mannose-binding lectin (MBL) gene polymorphisms were associated with susceptibility to SARS-CoV infection or disease severity in an ethnically homogeneous population born in northern China. Methods. The frequencies of 1 mutation in codon 54 and 3 promoter polymorphisms at nt -550, -221, and 4 were ascertained in 352 patients with SARS and 392 control subjects, by means of polymerase chain reaction direct sequencing. Results. Of 352 patients with SARS and 392 control subjects, 120 (34.4%) and 91 (23.2%) were carriers of the codon 54 variant, respectively (odds ratio [OR], 1.73 [95% confidence interval {CI}, 1.25-2.39]; P = .00086). A total of 123 (36.0%) of 352 patients with SARS and 100 (25.5%) of 392 control subjects had haplotype pairs associated with medium or low expression of MBL (OR, 1.67 [95% CI, 1.21-2.29]; P = .00187). The population-attributable fraction of patients with SARS that was associated with having the codon 54 variant was 20.1% (95% CI, 7.9%-32.3%). Conclusions. MBL gene polymorphisms were significantly associated with susceptibility to SARS-CoV infection; this might be explained by the reduced expression of functional MBL secondary to having the codon 54 variant.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0022-1899`
A02	`01`			`@0 JIDIAQ`
A03		`1`		`@0 J. infect. dis.`
A05				`@2 192`
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A08	`01`	`1`	`ENG`	`@1 Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection`
A11	`01`	`1`		`@1 HONGXING ZHANG`
A11	`02`	`1`		`@1 GANGQIAO ZHOU`
A11	`03`	`1`		`@1 LIANTENG ZHI`
A11	`04`	`1`		`@1 HAO YANG`
A11	`05`	`1`		`@1 YUN ZHAI`
A11	`06`	`1`		`@1 XIAOJIA DONG`
A11	`07`	`1`		`@1 XIUMEI ZHANG`
A11	`08`	`1`		`@1 XUE GAO`
A11	`09`	`1`		`@1 YUNPING ZHU`
A11	`10`	`1`		`@1 FUCHU HE`
A14	`01`			`@1 Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine @2 Beijing @3 CHN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 8 aut. @Z 9 aut. @Z 10 aut.`
A14	`02`			`@1 Chinese National Human Genome Center at Beijing @2 Beijing @3 CHN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut. @Z 10 aut.`
A14	`03`			`@1 Institute of Biophysics, Chinese Academy of Science @2 Beijing @3 CHN @Z 1 aut.`
A14	`04`			`@1 Institute of Biomedical Sciences, Fudan University @2 Shanghai @3 CHN @Z 10 aut.`
A20				`@1 1355-1361`
A21				`@1 2005`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 2052 @5 354000131975050060`
A44				`@0 0000 @1 © 2005 INIST-CNRS. All rights reserved.`
A45				`@0 39 ref.`
A47	`01`	`1`		`@0 05-0492671`
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A61				`@0 A`
A64	`01`	`1`		`@0 The Journal of infectious diseases`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 Background. Genetic determinants of susceptibility to severe acute respiratory syndrome coronavirus (SARS-CoV) infection remain unknown. We assessed whether mannose-binding lectin (MBL) gene polymorphisms were associated with susceptibility to SARS-CoV infection or disease severity in an ethnically homogeneous population born in northern China. Methods. The frequencies of 1 mutation in codon 54 and 3 promoter polymorphisms at nt -550, -221, and 4 were ascertained in 352 patients with SARS and 392 control subjects, by means of polymerase chain reaction direct sequencing. Results. Of 352 patients with SARS and 392 control subjects, 120 (34.4%) and 91 (23.2%) were carriers of the codon 54 variant, respectively (odds ratio [OR], 1.73 [95% confidence interval {CI}, 1.25-2.39]; P = .00086). A total of 123 (36.0%) of 352 patients with SARS and 100 (25.5%) of 392 control subjects had haplotype pairs associated with medium or low expression of MBL (OR, 1.67 [95% CI, 1.21-2.29]; P = .00187). The population-attributable fraction of patients with SARS that was associated with having the codon 54 variant was 20.1% (95% CI, 7.9%-32.3%). Conclusions. MBL gene polymorphisms were significantly associated with susceptibility to SARS-CoV infection; this might be explained by the reduced expression of functional MBL secondary to having the codon 54 variant.
C02	`01`	`X`		`@0 002A05C10`
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C03	`01`	`X`	`ENG`	`@0 Coronavirus @2 NW @5 01`
C03	`01`	`X`	`SPA`	`@0 Coronavirus @2 NW @5 01`
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C03	`05`	`X`	`FRE`	`@0 Microbiologie @5 08`
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C03	`05`	`X`	`SPA`	`@0 Microbiología @5 08`
C03	`06`	`X`	`FRE`	`@0 Infection @5 09`
C03	`06`	`X`	`ENG`	`@0 Infection @5 09`
C03	`06`	`X`	`SPA`	`@0 Infección @5 09`
C03	`07`	`X`	`FRE`	`@0 Syndrome respiratoire aigu sévère @2 NM @5 14`
C03	`07`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 14`
C03	`07`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 14`
C03	`08`	`X`	`FRE`	`@0 Association genetique @4 INC @5 79`
C07	`01`	`X`	`FRE`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`FRE`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`ENG`	`@0 Nidovirales @2 NW`
C07	`02`	`X`	`SPA`	`@0 Nidovirales @2 NW`
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C07	`05`	`X`	`FRE`	`@0 Virose`
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C07	`05`	`X`	`SPA`	`@0 Virosis`
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N21				`@1 346`
N44	`01`			`@1 OTO`
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Format Inist (serveur)

NO :	PASCAL 05-0492671 INIST
ET :	Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection
AU :	HONGXING ZHANG; GANGQIAO ZHOU; LIANTENG ZHI; HAO YANG; YUN ZHAI; XIAOJIA DONG; XIUMEI ZHANG; XUE GAO; YUNPING ZHU; FUCHU HE
AF :	Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine/Beijing/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 8 aut., 9 aut., 10 aut.); Chinese National Human Genome Center at Beijing/Beijing/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 10 aut.); Institute of Biophysics, Chinese Academy of Science/Beijing/Chine (1 aut.); Institute of Biomedical Sciences, Fudan University/Shanghai/Chine (10 aut.)
DT :	Publication en série; Niveau analytique
SO :	The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2005; Vol. 192; No. 8; Pp. 1355-1361; Bibl. 39 ref.
LA :	Anglais
EA :	Background. Genetic determinants of susceptibility to severe acute respiratory syndrome coronavirus (SARS-CoV) infection remain unknown. We assessed whether mannose-binding lectin (MBL) gene polymorphisms were associated with susceptibility to SARS-CoV infection or disease severity in an ethnically homogeneous population born in northern China. Methods. The frequencies of 1 mutation in codon 54 and 3 promoter polymorphisms at nt -550, -221, and 4 were ascertained in 352 patients with SARS and 392 control subjects, by means of polymerase chain reaction direct sequencing. Results. Of 352 patients with SARS and 392 control subjects, 120 (34.4%) and 91 (23.2%) were carriers of the codon 54 variant, respectively (odds ratio [OR], 1.73 [95% confidence interval {CI}, 1.25-2.39]; P = .00086). A total of 123 (36.0%) of 352 patients with SARS and 100 (25.5%) of 392 control subjects had haplotype pairs associated with medium or low expression of MBL (OR, 1.67 [95% CI, 1.21-2.29]; P = .00187). The population-attributable fraction of patients with SARS that was associated with having the codon 54 variant was 20.1% (95% CI, 7.9%-32.3%). Conclusions. MBL gene polymorphisms were significantly associated with susceptibility to SARS-CoV infection; this might be explained by the reduced expression of functional MBL secondary to having the codon 54 variant.
CC :	002A05C10; 002B05
FD :	Coronavirus; Mannose; Lectine; Polymorphisme; Microbiologie; Infection; Syndrome respiratoire aigu sévère; Association genetique
FG :	Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Poumon pathologie
ED :	Coronavirus; Mannose; Lectin; Polymorphism; Microbiology; Infection; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Lung disease
SD :	Coronavirus; Manosa; Lectina; Polimorfismo; Microbiología; Infección; Síndrome respiratorio agudo severo
LO :	INIST-2052.354000131975050060
ID :	05-0492671

Links to Exploration step

Pascal:05-0492671

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection</title>
<author><name sortKey="Hongxing Zhang" sort="Hongxing Zhang" uniqKey="Hongxing Zhang" last="Hongxing Zhang">HONGXING ZHANG</name>
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<author><name sortKey="Gangqiao Zhou" sort="Gangqiao Zhou" uniqKey="Gangqiao Zhou" last="Gangqiao Zhou">GANGQIAO ZHOU</name>
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<sZ>10 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>Chinese National Human Genome Center at Beijing</s1>
<s2>Beijing</s2>
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<author><name sortKey="Lianteng Zhi" sort="Lianteng Zhi" uniqKey="Lianteng Zhi" last="Lianteng Zhi">LIANTENG ZHI</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>Chinese National Human Genome Center at Beijing</s1>
<s2>Beijing</s2>
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</author>
<author><name sortKey="Hao Yang" sort="Hao Yang" uniqKey="Hao Yang" last="Hao Yang">HAO YANG</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
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<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
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</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Chinese National Human Genome Center at Beijing</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yun Zhai" sort="Yun Zhai" uniqKey="Yun Zhai" last="Yun Zhai">YUN ZHAI</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
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</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Chinese National Human Genome Center at Beijing</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Xiaojia Dong" sort="Xiaojia Dong" uniqKey="Xiaojia Dong" last="Xiaojia Dong">XIAOJIA DONG</name>
<affiliation><inist:fA14 i1="02"><s1>Chinese National Human Genome Center at Beijing</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Xiumei Zhang" sort="Xiumei Zhang" uniqKey="Xiumei Zhang" last="Xiumei Zhang">XIUMEI ZHANG</name>
<affiliation><inist:fA14 i1="02"><s1>Chinese National Human Genome Center at Beijing</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Xue Gao" sort="Xue Gao" uniqKey="Xue Gao" last="Xue Gao">XUE GAO</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Yunping Zhu" sort="Yunping Zhu" uniqKey="Yunping Zhu" last="Yunping Zhu">YUNPING ZHU</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fuchu He" sort="Fuchu He" uniqKey="Fuchu He" last="Fuchu He">FUCHU HE</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Chinese National Human Genome Center at Beijing</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>Institute of Biomedical Sciences, Fudan University</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">The Journal of infectious diseases</title>
<title level="j" type="abbreviated">J. infect. dis.</title>
<idno type="ISSN">0022-1899</idno>
<imprint><date when="2005">2005</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">The Journal of infectious diseases</title>
<title level="j" type="abbreviated">J. infect. dis.</title>
<idno type="ISSN">0022-1899</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Coronavirus</term>
<term>Infection</term>
<term>Lectin</term>
<term>Mannose</term>
<term>Microbiology</term>
<term>Polymorphism</term>
<term>Severe acute respiratory syndrome</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Coronavirus</term>
<term>Mannose</term>
<term>Lectine</term>
<term>Polymorphisme</term>
<term>Microbiologie</term>
<term>Infection</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Association genetique</term>
</keywords>
</textClass>
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<front><div type="abstract" xml:lang="en">Background. Genetic determinants of susceptibility to severe acute respiratory syndrome coronavirus (SARS-CoV) infection remain unknown. We assessed whether mannose-binding lectin (MBL) gene polymorphisms were associated with susceptibility to SARS-CoV infection or disease severity in an ethnically homogeneous population born in northern China. Methods. The frequencies of 1 mutation in codon 54 and 3 promoter polymorphisms at nt -550, -221, and 4 were ascertained in 352 patients with SARS and 392 control subjects, by means of polymerase chain reaction direct sequencing. Results. Of 352 patients with SARS and 392 control subjects, 120 (34.4%) and 91 (23.2%) were carriers of the codon 54 variant, respectively (odds ratio [OR], 1.73 [95% confidence interval {CI}, 1.25-2.39]; P = .00086). A total of 123 (36.0%) of 352 patients with SARS and 100 (25.5%) of 392 control subjects had haplotype pairs associated with medium or low expression of MBL (OR, 1.67 [95% CI, 1.21-2.29]; P = .00187). The population-attributable fraction of patients with SARS that was associated with having the codon 54 variant was 20.1% (95% CI, 7.9%-32.3%). Conclusions. MBL gene polymorphisms were significantly associated with susceptibility to SARS-CoV infection; this might be explained by the reduced expression of functional MBL secondary to having the codon 54 variant.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-1899</s0>
</fA01>
<fA02 i1="01"><s0>JIDIAQ</s0>
</fA02>
<fA03 i2="1"><s0>J. infect. dis.</s0>
</fA03>
<fA05><s2>192</s2>
</fA05>
<fA06><s2>8</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>HONGXING ZHANG</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>GANGQIAO ZHOU</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>LIANTENG ZHI</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>HAO YANG</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>YUN ZHAI</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>XIAOJIA DONG</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>XIUMEI ZHANG</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>XUE GAO</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>YUNPING ZHU</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>FUCHU HE</s1>
</fA11>
<fA14 i1="01"><s1>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Chinese National Human Genome Center at Beijing</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Institute of Biophysics, Chinese Academy of Science</s1>
<s2>Beijing</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Institute of Biomedical Sciences, Fudan University</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA20><s1>1355-1361</s1>
</fA20>
<fA21><s1>2005</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>2052</s2>
<s5>354000131975050060</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2005 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>39 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>05-0492671</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>The Journal of infectious diseases</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Background. Genetic determinants of susceptibility to severe acute respiratory syndrome coronavirus (SARS-CoV) infection remain unknown. We assessed whether mannose-binding lectin (MBL) gene polymorphisms were associated with susceptibility to SARS-CoV infection or disease severity in an ethnically homogeneous population born in northern China. Methods. The frequencies of 1 mutation in codon 54 and 3 promoter polymorphisms at nt -550, -221, and 4 were ascertained in 352 patients with SARS and 392 control subjects, by means of polymerase chain reaction direct sequencing. Results. Of 352 patients with SARS and 392 control subjects, 120 (34.4%) and 91 (23.2%) were carriers of the codon 54 variant, respectively (odds ratio [OR], 1.73 [95% confidence interval {CI}, 1.25-2.39]; P = .00086). A total of 123 (36.0%) of 352 patients with SARS and 100 (25.5%) of 392 control subjects had haplotype pairs associated with medium or low expression of MBL (OR, 1.67 [95% CI, 1.21-2.29]; P = .00187). The population-attributable fraction of patients with SARS that was associated with having the codon 54 variant was 20.1% (95% CI, 7.9%-32.3%). Conclusions. MBL gene polymorphisms were significantly associated with susceptibility to SARS-CoV infection; this might be explained by the reduced expression of functional MBL secondary to having the codon 54 variant.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A05C10</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B05</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Coronavirus</s0>
<s2>NW</s2>
<s5>01</s5>
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<fC03 i1="02" i2="X" l="FRE"><s0>Mannose</s0>
<s2>NK</s2>
<s5>05</s5>
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<fC03 i1="02" i2="X" l="ENG"><s0>Mannose</s0>
<s2>NK</s2>
<s5>05</s5>
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<fC03 i1="02" i2="X" l="SPA"><s0>Manosa</s0>
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<s5>06</s5>
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<fC03 i1="04" i2="X" l="FRE"><s0>Polymorphisme</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Polymorphism</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Polimorfismo</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Microbiologie</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Microbiology</s0>
<s5>08</s5>
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<s5>08</s5>
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<s5>09</s5>
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<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Syndrome respiratoire aigu sévère</s0>
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<s5>14</s5>
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<fC03 i1="07" i2="X" l="ENG"><s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
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<s5>79</s5>
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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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<s2>NW</s2>
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<s2>NW</s2>
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<s2>NW</s2>
</fC07>
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<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
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<fC07 i1="04" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>13</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>13</s5>
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<fC07 i1="05" i2="X" l="SPA"><s0>Virosis</s0>
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<s5>16</s5>
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<s5>16</s5>
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<s5>16</s5>
</fC07>
<fN21><s1>346</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
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<server><NO>PASCAL 05-0492671 INIST</NO>
<ET>Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection</ET>
<AU>HONGXING ZHANG; GANGQIAO ZHOU; LIANTENG ZHI; HAO YANG; YUN ZHAI; XIAOJIA DONG; XIUMEI ZHANG; XUE GAO; YUNPING ZHU; FUCHU HE</AU>
<AF>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine/Beijing/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 8 aut., 9 aut., 10 aut.); Chinese National Human Genome Center at Beijing/Beijing/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 10 aut.); Institute of Biophysics, Chinese Academy of Science/Beijing/Chine (1 aut.); Institute of Biomedical Sciences, Fudan University/Shanghai/Chine (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2005; Vol. 192; No. 8; Pp. 1355-1361; Bibl. 39 ref.</SO>
<LA>Anglais</LA>
<EA>Background. Genetic determinants of susceptibility to severe acute respiratory syndrome coronavirus (SARS-CoV) infection remain unknown. We assessed whether mannose-binding lectin (MBL) gene polymorphisms were associated with susceptibility to SARS-CoV infection or disease severity in an ethnically homogeneous population born in northern China. Methods. The frequencies of 1 mutation in codon 54 and 3 promoter polymorphisms at nt -550, -221, and 4 were ascertained in 352 patients with SARS and 392 control subjects, by means of polymerase chain reaction direct sequencing. Results. Of 352 patients with SARS and 392 control subjects, 120 (34.4%) and 91 (23.2%) were carriers of the codon 54 variant, respectively (odds ratio [OR], 1.73 [95% confidence interval {CI}, 1.25-2.39]; P = .00086). A total of 123 (36.0%) of 352 patients with SARS and 100 (25.5%) of 392 control subjects had haplotype pairs associated with medium or low expression of MBL (OR, 1.67 [95% CI, 1.21-2.29]; P = .00187). The population-attributable fraction of patients with SARS that was associated with having the codon 54 variant was 20.1% (95% CI, 7.9%-32.3%). Conclusions. MBL gene polymorphisms were significantly associated with susceptibility to SARS-CoV infection; this might be explained by the reduced expression of functional MBL secondary to having the codon 54 variant.</EA>
<CC>002A05C10; 002B05</CC>
<FD>Coronavirus; Mannose; Lectine; Polymorphisme; Microbiologie; Infection; Syndrome respiratoire aigu sévère; Association genetique</FD>
<FG>Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Poumon pathologie</FG>
<ED>Coronavirus; Mannose; Lectin; Polymorphism; Microbiology; Infection; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Lung disease</EG>
<SD>Coronavirus; Manosa; Lectina; Polimorfismo; Microbiología; Infección; Síndrome respiratorio agudo severo</SD>
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   |texte=   Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection
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Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection

Association between mannose-binding lectin gene polymorphisms and susceptibility to severe acute respiratory syndrome coronavirus infection

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