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Article: Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection
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TitleMannose-binding lectin in severe acute respiratory syndrome coronavirus infection
 
AuthorsIp, WKE3 1
Kwok, HC3
Law, HKW3
Tso, GHW3
Kong, EKP3
Wong, WHS3
Yuk, FT3
Yung, RWH5
Chow, EY9
Ka, LA6
Chan, EYT7
Lim, W8
Jensenius, JC2
Turner, MW4
Peiris, JSM3
Yu, LL3 3
 
Issue Date2005
 
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
 
CitationJournal Of Infectious Diseases, 2005, v. 191 n. 10, p. 1697-1704 [How to Cite?]
DOI: http://dx.doi.org/10.1086/429631
 
AbstractLittle 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. © 2005 by the Infectious Diseases Society of America. All rights reserved.
 
ISSN0022-1899
2012 Impact Factor: 5.848
2012 SCImago Journal Rankings: 2.723
 
DOIhttp://dx.doi.org/10.1086/429631
 
ISI Accession Number IDWOS:000228465000016
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorIp, WKE
 
dc.contributor.authorKwok, HC
 
dc.contributor.authorLaw, HKW
 
dc.contributor.authorTso, GHW
 
dc.contributor.authorKong, EKP
 
dc.contributor.authorWong, WHS
 
dc.contributor.authorYuk, FT
 
dc.contributor.authorYung, RWH
 
dc.contributor.authorChow, EY
 
dc.contributor.authorKa, LA
 
dc.contributor.authorChan, EYT
 
dc.contributor.authorLim, W
 
dc.contributor.authorJensenius, JC
 
dc.contributor.authorTurner, MW
 
dc.contributor.authorPeiris, JSM
 
dc.contributor.authorYu, LL
 
dc.date.accessioned2007-03-23T04:39:48Z
 
dc.date.available2007-03-23T04:39:48Z
 
dc.date.issued2005
 
dc.description.abstractLittle 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. © 2005 by the Infectious Diseases Society of America. All rights reserved.
 
dc.description.naturepublished_or_final_version
 
dc.format.extent1018712 bytes
 
dc.format.extent25600 bytes
 
dc.format.extent2912 bytes
 
dc.format.mimetypeapplication/pdf
 
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dc.identifier.citationJournal Of Infectious Diseases, 2005, v. 191 n. 10, p. 1697-1704 [How to Cite?]
DOI: http://dx.doi.org/10.1086/429631
 
dc.identifier.citeulike4502907
 
dc.identifier.doihttp://dx.doi.org/10.1086/429631
 
dc.identifier.epage1704
 
dc.identifier.hkuros97751
 
dc.identifier.isiWOS:000228465000016
 
dc.identifier.issn0022-1899
2012 Impact Factor: 5.848
2012 SCImago Journal Rankings: 2.723
 
dc.identifier.issue10
 
dc.identifier.openurl
 
dc.identifier.pmid15838797
 
dc.identifier.scopuseid_2-s2.0-20844452048
 
dc.identifier.spage1697
 
dc.identifier.urihttp://hdl.handle.net/10722/43141
 
dc.identifier.volume191
 
dc.languageeng
 
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Infectious Diseases
 
dc.relation.referencesReferences in Scopus
 
dc.rightsJournal of Infectious Diseases. Copyright © University of Chicago Press.
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshGenetic predisposition to disease
 
dc.subject.meshMannose-binding lectin - blood - genetics
 
dc.subject.meshProtein binding
 
dc.subject.meshComplement activation
 
dc.subject.meshSevere acute respiratory syndrome
 
dc.titleMannose-binding lectin in severe acute respiratory syndrome coronavirus infection
 
dc.typeArticle
 
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Author Affiliations
  1. Massachusetts General Hospital
  2. Aarhus Universitet
  3. The University of Hong Kong
  4. UCL Institute of Child Health
  5. Pamela Youde Nethersole Eastern Hospital
  6. Princess Margaret Hospital
  7. Queen Mary Hospital Hong Kong
  8. Government Virus Unit
  9. United Christian Hospital