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Article: Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection

TitleMannose-binding lectin in severe acute respiratory syndrome coronavirus infection
Authors
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2005, v. 191 n. 10, p. 1697-1704 How to Cite?
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. © 2005 by the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/43141
ISSN
2013 Impact Factor: 5.778
ISI Accession Number ID
References

 

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
DC FieldValueLanguage
dc.contributor.authorIp, WKEen_HK
dc.contributor.authorKwok, HCen_HK
dc.contributor.authorLaw, HKWen_HK
dc.contributor.authorTso, GHWen_HK
dc.contributor.authorKong, EKPen_HK
dc.contributor.authorWong, WHSen_HK
dc.contributor.authorYuk, FTen_HK
dc.contributor.authorYung, RWHen_HK
dc.contributor.authorChow, EYen_HK
dc.contributor.authorKa, LAen_HK
dc.contributor.authorChan, EYTen_HK
dc.contributor.authorLim, Wen_HK
dc.contributor.authorJensenius, JCen_HK
dc.contributor.authorTurner, MWen_HK
dc.contributor.authorPeiris, JSMen_HK
dc.contributor.authorYu, LLen_HK
dc.date.accessioned2007-03-23T04:39:48Z-
dc.date.available2007-03-23T04:39:48Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2005, v. 191 n. 10, p. 1697-1704en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/43141-
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.en_HK
dc.format.extent1018712 bytes-
dc.format.extent25600 bytes-
dc.format.extent2912 bytes-
dc.format.mimetypeapplication/pdf-
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dc.format.mimetypetext/plain-
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org en_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.rightsJournal of Infectious Diseases. Copyright © University of Chicago Press.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshGenetic predisposition to diseaseen_HK
dc.subject.meshMannose-binding lectin - blood - geneticsen_HK
dc.subject.meshProtein bindingen_HK
dc.subject.meshComplement activationen_HK
dc.subject.meshSevere acute respiratory syndromeen_HK
dc.titleMannose-binding lectin in severe acute respiratory syndrome coronavirus infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1899&volume=191&issue=10&spage=1697&epage=1704&date=2005&atitle=Mannose-Binding+Lectin+in+Severe+Acute+Respiratory+Syndrome+Coronavirus+Infectionen_HK
dc.identifier.emailPeiris, JSM: malik@hkucc.hku.hken_HK
dc.identifier.authorityPeiris, JSM=rp00410en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1086/429631en_HK
dc.identifier.pmid15838797en_HK
dc.identifier.scopuseid_2-s2.0-20844452048en_HK
dc.identifier.hkuros97751-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-20844452048&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume191en_HK
dc.identifier.issue10en_HK
dc.identifier.spage1697en_HK
dc.identifier.epage1704en_HK
dc.identifier.isiWOS:000228465000016-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridIp, WKE=35083568800en_HK
dc.identifier.scopusauthoridKwok, HC=8617702800en_HK
dc.identifier.scopusauthoridLaw, HKW=7101939394en_HK
dc.identifier.scopusauthoridTso, GHW=8617703000en_HK
dc.identifier.scopusauthoridKong, EKP=8617703100en_HK
dc.identifier.scopusauthoridWong, WHS=13310222200en_HK
dc.identifier.scopusauthoridYuk, FT=8617703300en_HK
dc.identifier.scopusauthoridYung, RWH=7005594277en_HK
dc.identifier.scopusauthoridChow, EY=7102595571en_HK
dc.identifier.scopusauthoridKa, LA=8617703600en_HK
dc.identifier.scopusauthoridChan, EYT=7401994013en_HK
dc.identifier.scopusauthoridLim, W=7202378277en_HK
dc.identifier.scopusauthoridJensenius, JC=7005603928en_HK
dc.identifier.scopusauthoridTurner, MW=7403215582en_HK
dc.identifier.scopusauthoridPeiris, JSM=7005486823en_HK
dc.identifier.scopusauthoridYu, LL=8617704200en_HK
dc.identifier.citeulike4502907-

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