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Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection

Identifieur interne : 004D95 ( Main/Exploration ); précédent : 004D94; suivant : 004D96

Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection

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

Source :

RBID : Pascal:05-0272904

Descripteurs français

English descriptors

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.


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Le document en format XML

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<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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<name sortKey="Yu Lung Lau" sort="Yu Lung Lau" uniqKey="Yu Lung Lau" last="Yu Lung Lau">YU LUNG LAU</name>
<affiliation wicri:level="1">
<inist:fA14 i1="01">
<s1>Department of Paediatrics and Adolescent Medicine, The University of Hong Kong</s1>
<s3>HKG</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
<country>Hong Kong</country>
<wicri:noRegion>Department of Paediatrics and Adolescent Medicine, The University of Hong Kong</wicri:noRegion>
</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>Severe acute respiratory syndrome</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Coronavirus</term>
<term>Mannose</term>
<term>Lectine</term>
<term>Microbiologie</term>
<term>Infection</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<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>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Danemark</li>
<li>Hong Kong</li>
<li>Royaume-Uni</li>
</country>
<region>
<li>Angleterre</li>
<li>Grand Londres</li>
</region>
<settlement>
<li>Londres</li>
</settlement>
<orgName>
<li>University College de Londres</li>
</orgName>
</list>
<tree>
<country name="Hong Kong">
<noRegion>
<name sortKey="Eddie Ip, W K" sort="Eddie Ip, W K" uniqKey="Eddie Ip W" first="W. K." last="Eddie Ip">W. K. Eddie Ip</name>
</noRegion>
<name sortKey="Chan, Eric Y T" sort="Chan, Eric Y T" uniqKey="Chan E" first="Eric Y. T." last="Chan">Eric Y. T. Chan</name>
<name sortKey="Chow, Eudora Y" sort="Chow, Eudora Y" uniqKey="Chow E" first="Eudora Y." last="Chow">Eudora Y. Chow</name>
<name sortKey="Ka Leung Au" sort="Ka Leung Au" uniqKey="Ka Leung Au" last="Ka Leung Au">KA LEUNG AU</name>
<name sortKey="Kong, Eric K P" sort="Kong, Eric K P" uniqKey="Kong E" first="Eric K. P." last="Kong">Eric K. P. Kong</name>
<name sortKey="Kwok Hung Chan" sort="Kwok Hung Chan" uniqKey="Kwok Hung Chan" last="Kwok Hung Chan">KWOK HUNG CHAN</name>
<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>
<name sortKey="Lim, Wilina" sort="Lim, Wilina" uniqKey="Lim W" first="Wilina" last="Lim">Wilina Lim</name>
<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>
<name sortKey="Tso, Gloria H W" sort="Tso, Gloria H W" uniqKey="Tso G" first="Gloria H. W." last="Tso">Gloria H. W. Tso</name>
<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>
<name sortKey="Yu Lung Lau" sort="Yu Lung Lau" uniqKey="Yu Lung Lau" last="Yu Lung Lau">YU LUNG LAU</name>
<name sortKey="Yuk Fai To" sort="Yuk Fai To" uniqKey="Yuk Fai To" last="Yuk Fai To">YUK FAI TO</name>
<name sortKey="Yung, Raymond W H" sort="Yung, Raymond W H" uniqKey="Yung R" first="Raymond W. H." last="Yung">Raymond W. H. Yung</name>
</country>
<country name="Danemark">
<noRegion>
<name sortKey="Jensenius, Jens C" sort="Jensenius, Jens C" uniqKey="Jensenius J" first="Jens C." last="Jensenius">Jens C. Jensenius</name>
</noRegion>
</country>
<country name="Royaume-Uni">
<region name="Angleterre">
<name sortKey="Turner, Malcolm W" sort="Turner, Malcolm W" uniqKey="Turner M" first="Malcolm W." last="Turner">Malcolm W. Turner</name>
</region>
</country>
</tree>
</affiliations>
</record>

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