SrasV1, PascalFrancis, Corpus, bibRecord, 000660

Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection

Identifieur interne : 000660 ( PascalFrancis/Corpus ); précédent : 000659; suivant : 000661

Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection

Auteurs : W. K. Eddie Ip ; KWOK HUNG CHAN ; Helen K. W. Law ; Gloria H. W. Tso ; Eric K. P. Kong ; Wilfred H. S. Wong ; YUK FAI TO ; Raymond W. H. Yung ; Eudora Y. Chow ; KA LEUNG AU ; Eric Y. T. Chan ; Wilina Lim ; Jens C. Jensenius ; Malcolm W. Turner ; J. S. Malik Peiris ; YU LUNG LAU

Source :

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

RBID : Pascal:05-0272904

Descripteurs français

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

English descriptors

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

Abstract

Little is known about the innate immune response to severe acute respiratory syndrome (SARS) coronavirus (CoV) infection. Mannose-binding lectin (MBL), a key molecule in innate immunity, functions as an ante-antibody before the specific antibody response. Here, we describe a case-control study that included 569 patients with SARS and 1188 control subjects and used in vitro assays to investigate the role that MBL plays in SARS-CoV infection. The distribution of MBL gene polymorphisms was significantly different between patients with SARS and control subjects, with a higher frequency of haplotypes associated with low or deficient serum levels of MBL in patients with SARS than in control subjects. Serum levels of MBL were also significantly lower in patients with SARS than in control subjects. There was, however, no association between MBL genotypes, which are associated with low or deficient serum levels of MBL, and mortality related to SARS. MBL could bind SARS-CoV in a dose- and calcium-dependent and mannan-inhibitable fashion in vitro, suggesting that binding is through the carbohydrate recognition domains of MBL. Furthermore, deposition of complement C4 on SARS-CoV was enhanced by MBL. Inhibition of the infectivity of SARS-CoV by MBL in fetal rhesus kidney cells (FRhK-4) was also observed. These results suggest that MBL contributes to the first-line host defense against SARS-CoV and that MBL deficiency is a susceptibility factor for acquisition of SARS.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`03`	`1`		`@1 LAW (Helen K. W.)`
A11	`04`	`1`		`@1 TSO (Gloria H. W.)`
A11	`05`	`1`		`@1 KONG (Eric K. P.)`
A11	`06`	`1`		`@1 WONG (Wilfred H. S.)`
A11	`07`	`1`		`@1 YUK FAI TO`
A11	`08`	`1`		`@1 YUNG (Raymond W. H.)`
A11	`09`	`1`		`@1 CHOW (Eudora Y.)`
A11	`10`	`1`		`@1 KA LEUNG AU`
A11	`11`	`1`		`@1 CHAN (Eric Y. T.)`
A11	`12`	`1`		`@1 LIM (Wilina)`
A11	`13`	`1`		`@1 JENSENIUS (Jens C.)`
A11	`14`	`1`		`@1 TURNER (Malcolm W.)`
A11	`15`	`1`		`@1 MALIK PEIRIS (J. S.)`
A11	`16`	`1`		`@1 YU LUNG LAU`
A14	`01`			`@1 Department of Paediatrics and Adolescent Medicine, The University of Hong Kong @3 HKG @Z 1 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut. @Z 16 aut.`
A14	`02`			`@1 Department of Microbiology, The University of Hong Kong @3 HKG @Z 2 aut. @Z 15 aut.`
A14	`03`			`@1 Department of Pathology, Pamela Nethersole Youde Hospital @3 HKG @Z 8 aut.`
A14	`04`			`@1 United Christian Hospital @3 HKG @Z 9 aut.`
A14	`05`			`@1 Princess Margaret Hospital @3 HKG @Z 10 aut.`
A14	`06`			`@1 Queen Mary Hospital @3 HKG @Z 11 aut.`
A14	`07`			`@1 Government Virus Unit, Department of Health @3 HKG @Z 12 aut.`
A14	`08`			`@1 Department of Medical Microbiology and Immunology, University of Aarhus @3 DNK @Z 13 aut.`
A14	`09`			`@1 Immunobiology Unit, Institute of Child Health, University College London @2 London @3 GBR @Z 14 aut.`
A20				`@1 1697-1704`
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A64	`01`	`1`		`@0 The Journal of infectious diseases`
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C01	`01`		`ENG`	@0 Little is known about the innate immune response to severe acute respiratory syndrome (SARS) coronavirus (CoV) infection. Mannose-binding lectin (MBL), a key molecule in innate immunity, functions as an ante-antibody before the specific antibody response. Here, we describe a case-control study that included 569 patients with SARS and 1188 control subjects and used in vitro assays to investigate the role that MBL plays in SARS-CoV infection. The distribution of MBL gene polymorphisms was significantly different between patients with SARS and control subjects, with a higher frequency of haplotypes associated with low or deficient serum levels of MBL in patients with SARS than in control subjects. Serum levels of MBL were also significantly lower in patients with SARS than in control subjects. There was, however, no association between MBL genotypes, which are associated with low or deficient serum levels of MBL, and mortality related to SARS. MBL could bind SARS-CoV in a dose- and calcium-dependent and mannan-inhibitable fashion in vitro, suggesting that binding is through the carbohydrate recognition domains of MBL. Furthermore, deposition of complement C4 on SARS-CoV was enhanced by MBL. Inhibition of the infectivity of SARS-CoV by MBL in fetal rhesus kidney cells (FRhK-4) was also observed. These results suggest that MBL contributes to the first-line host defense against SARS-CoV and that MBL deficiency is a susceptibility factor for acquisition of SARS.
C02	`01`	`X`		`@0 002A05C10`
C02	`02`	`X`		`@0 002B05`
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C03	`01`	`X`	`ENG`	`@0 Coronavirus @2 NW @5 01`
C03	`01`	`X`	`SPA`	`@0 Coronavirus @2 NW @5 01`
C03	`02`	`X`	`FRE`	`@0 Mannose @2 NK @5 05`
C03	`02`	`X`	`ENG`	`@0 Mannose @2 NK @5 05`
C03	`02`	`X`	`SPA`	`@0 Manosa @2 NK @5 05`
C03	`03`	`X`	`FRE`	`@0 Lectine @5 06`
C03	`03`	`X`	`ENG`	`@0 Lectin @5 06`
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C03	`04`	`X`	`SPA`	`@0 Microbiología @5 07`
C03	`05`	`X`	`FRE`	`@0 Infection @5 08`
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C03	`05`	`X`	`SPA`	`@0 Infección @5 08`
C03	`06`	`X`	`FRE`	`@0 Syndrome respiratoire aigu sévère @2 NM @5 14`
C03	`06`	`X`	`ENG`	`@0 Severe acute respiratory syndrome @2 NM @5 14`
C03	`06`	`X`	`SPA`	`@0 Síndrome respiratorio agudo severo @2 NM @5 14`
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C07	`01`	`X`	`ENG`	`@0 Coronaviridae @2 NW`
C07	`01`	`X`	`SPA`	`@0 Coronaviridae @2 NW`
C07	`02`	`X`	`FRE`	`@0 Nidovirales @2 NW`
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C07	`03`	`X`	`FRE`	`@0 Virus @2 NW`
C07	`03`	`X`	`ENG`	`@0 Virus @2 NW`
C07	`03`	`X`	`SPA`	`@0 Virus @2 NW`
C07	`04`	`X`	`FRE`	`@0 Appareil respiratoire pathologie @5 13`
C07	`04`	`X`	`ENG`	`@0 Respiratory disease @5 13`
C07	`04`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 13`
C07	`05`	`X`	`FRE`	`@0 Virose`
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C07	`06`	`X`	`SPA`	`@0 Pulmón patología @5 16`
N21				`@1 192`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 05-0272904 INIST
ET :	Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection
AU :	EDDIE IP (W. K.); KWOK HUNG CHAN; LAW (Helen K. W.); TSO (Gloria H. W.); KONG (Eric K. P.); WONG (Wilfred H. S.); YUK FAI TO; YUNG (Raymond W. H.); CHOW (Eudora Y.); KA LEUNG AU; CHAN (Eric Y. T.); LIM (Wilina); JENSENIUS (Jens C.); TURNER (Malcolm W.); MALIK PEIRIS (J. S.); YU LUNG LAU
AF :	Department of Paediatrics and Adolescent Medicine, The University of Hong Kong/Hong-Kong (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 16 aut.); Department of Microbiology, The University of Hong Kong/Hong-Kong (2 aut., 15 aut.); Department of Pathology, Pamela Nethersole Youde Hospital/Hong-Kong (8 aut.); United Christian Hospital/Hong-Kong (9 aut.); Princess Margaret Hospital/Hong-Kong (10 aut.); Queen Mary Hospital/Hong-Kong (11 aut.); Government Virus Unit, Department of Health/Hong-Kong (12 aut.); Department of Medical Microbiology and Immunology, University of Aarhus/Danemark (13 aut.); Immunobiology Unit, Institute of Child Health, University College London/London/Royaume-Uni (14 aut.)
DT :	Publication en série; Niveau analytique
SO :	The Journal of infectious diseases; ISSN 0022-1899; Coden JIDIAQ; Etats-Unis; Da. 2005; Vol. 191; No. 10; Pp. 1697-1704; Bibl. 47 ref.
LA :	Anglais
EA :	Little is known about the innate immune response to severe acute respiratory syndrome (SARS) coronavirus (CoV) infection. Mannose-binding lectin (MBL), a key molecule in innate immunity, functions as an ante-antibody before the specific antibody response. Here, we describe a case-control study that included 569 patients with SARS and 1188 control subjects and used in vitro assays to investigate the role that MBL plays in SARS-CoV infection. The distribution of MBL gene polymorphisms was significantly different between patients with SARS and control subjects, with a higher frequency of haplotypes associated with low or deficient serum levels of MBL in patients with SARS than in control subjects. Serum levels of MBL were also significantly lower in patients with SARS than in control subjects. There was, however, no association between MBL genotypes, which are associated with low or deficient serum levels of MBL, and mortality related to SARS. MBL could bind SARS-CoV in a dose- and calcium-dependent and mannan-inhibitable fashion in vitro, suggesting that binding is through the carbohydrate recognition domains of MBL. Furthermore, deposition of complement C4 on SARS-CoV was enhanced by MBL. Inhibition of the infectivity of SARS-CoV by MBL in fetal rhesus kidney cells (FRhK-4) was also observed. These results suggest that MBL contributes to the first-line host defense against SARS-CoV and that MBL deficiency is a susceptibility factor for acquisition of SARS.
CC :	002A05C10; 002B05
FD :	Coronavirus; Mannose; Lectine; Microbiologie; Infection; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Virose; Poumon pathologie
ED :	Coronavirus; Mannose; Lectin; Microbiology; Infection; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Respiratory disease; Viral disease; Lung disease
SD :	Coronavirus; Manosa; Lectina; Microbiología; Infección; Síndrome respiratorio agudo severo
LO :	INIST-2052.354000124939620150
ID :	05-0272904

Links to Exploration step

Pascal:05-0272904

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection</title>
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<author><name sortKey="Kwok Hung Chan" sort="Kwok Hung Chan" uniqKey="Kwok Hung Chan" last="Kwok Hung Chan">KWOK HUNG CHAN</name>
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<author><name sortKey="Law, Helen K W" sort="Law, Helen K W" uniqKey="Law H" first="Helen K. W." last="Law">Helen K. W. Law</name>
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<author><name sortKey="Wong, Wilfred H S" sort="Wong, Wilfred H S" uniqKey="Wong W" first="Wilfred H. S." last="Wong">Wilfred H. S. Wong</name>
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<author><name sortKey="Malik Peiris, J S" sort="Malik Peiris, J S" uniqKey="Malik Peiris J" first="J. S." last="Malik Peiris">J. S. Malik Peiris</name>
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<author><name sortKey="Yu Lung Lau" sort="Yu Lung Lau" uniqKey="Yu Lung Lau" last="Yu Lung Lau">YU LUNG LAU</name>
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<front><div type="abstract" xml:lang="en">Little is known about the innate immune response to severe acute respiratory syndrome (SARS) coronavirus (CoV) infection. Mannose-binding lectin (MBL), a key molecule in innate immunity, functions as an ante-antibody before the specific antibody response. Here, we describe a case-control study that included 569 patients with SARS and 1188 control subjects and used in vitro assays to investigate the role that MBL plays in SARS-CoV infection. The distribution of MBL gene polymorphisms was significantly different between patients with SARS and control subjects, with a higher frequency of haplotypes associated with low or deficient serum levels of MBL in patients with SARS than in control subjects. Serum levels of MBL were also significantly lower in patients with SARS than in control subjects. There was, however, no association between MBL genotypes, which are associated with low or deficient serum levels of MBL, and mortality related to SARS. MBL could bind SARS-CoV in a dose- and calcium-dependent and mannan-inhibitable fashion in vitro, suggesting that binding is through the carbohydrate recognition domains of MBL. Furthermore, deposition of complement C4 on SARS-CoV was enhanced by MBL. Inhibition of the infectivity of SARS-CoV by MBL in fetal rhesus kidney cells (FRhK-4) was also observed. These results suggest that MBL contributes to the first-line host defense against SARS-CoV and that MBL deficiency is a susceptibility factor for acquisition of SARS.</div>
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<ET>Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection</ET>
<AU>EDDIE IP (W. K.); KWOK HUNG CHAN; LAW (Helen K. W.); TSO (Gloria H. W.); KONG (Eric K. P.); WONG (Wilfred H. S.); YUK FAI TO; YUNG (Raymond W. H.); CHOW (Eudora Y.); KA LEUNG AU; CHAN (Eric Y. T.); LIM (Wilina); JENSENIUS (Jens C.); TURNER (Malcolm W.); MALIK PEIRIS (J. S.); YU LUNG LAU</AU>
<AF>Department of Paediatrics and Adolescent Medicine, The University of Hong Kong/Hong-Kong (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 16 aut.); Department of Microbiology, The University of Hong Kong/Hong-Kong (2 aut., 15 aut.); Department of Pathology, Pamela Nethersole Youde Hospital/Hong-Kong (8 aut.); United Christian Hospital/Hong-Kong (9 aut.); Princess Margaret Hospital/Hong-Kong (10 aut.); Queen Mary Hospital/Hong-Kong (11 aut.); Government Virus Unit, Department of Health/Hong-Kong (12 aut.); Department of Medical Microbiology and Immunology, University of Aarhus/Danemark (13 aut.); Immunobiology Unit, Institute of Child Health, University College London/London/Royaume-Uni (14 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. 191; No. 10; Pp. 1697-1704; Bibl. 47 ref.</SO>
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<EA>Little is known about the innate immune response to severe acute respiratory syndrome (SARS) coronavirus (CoV) infection. Mannose-binding lectin (MBL), a key molecule in innate immunity, functions as an ante-antibody before the specific antibody response. Here, we describe a case-control study that included 569 patients with SARS and 1188 control subjects and used in vitro assays to investigate the role that MBL plays in SARS-CoV infection. The distribution of MBL gene polymorphisms was significantly different between patients with SARS and control subjects, with a higher frequency of haplotypes associated with low or deficient serum levels of MBL in patients with SARS than in control subjects. Serum levels of MBL were also significantly lower in patients with SARS than in control subjects. There was, however, no association between MBL genotypes, which are associated with low or deficient serum levels of MBL, and mortality related to SARS. MBL could bind SARS-CoV in a dose- and calcium-dependent and mannan-inhibitable fashion in vitro, suggesting that binding is through the carbohydrate recognition domains of MBL. Furthermore, deposition of complement C4 on SARS-CoV was enhanced by MBL. Inhibition of the infectivity of SARS-CoV by MBL in fetal rhesus kidney cells (FRhK-4) was also observed. These results suggest that MBL contributes to the first-line host defense against SARS-CoV and that MBL deficiency is a susceptibility factor for acquisition of SARS.</EA>
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Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection

Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection

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