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Article: Mannose-binding lectin in chronic hepatitis B virus infection

TitleMannose-binding lectin in chronic hepatitis B virus infection
Authors
Issue Date2005
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2005, v. 42 n. 5, p. 1037-1045 How to Cite?
AbstractMannose binding lectin (MBL) is a pattern-recognition molecule of the innate immune system. The roles of MBL and its gene (mbl2) polymorphisms, - 221X/Y and codon 54A/B, in hepatitis B virus (HBV) infection were investigated in this study. We recruited 320 nonprogressed hepatitis B surface antigen (HBsAg) carriers; 199 progressed HBsAg carriers with hepatocellular carcinoma or cirrhosis; 87 spontaneously recovered individuals who were HBsAg negative and anti-HBs and anti HBc positive; and 484 controls who were naïve to HBV. There was no significant difference between nonprogressed carriers, spontaneously recovered individuals, and controls in terms of serum MBL levels and mbl2 polymorphisms distributions. However, the low MBL genotypes had a dose-dependent correlation with the cirrhosis and hepatocellular carcinoma in progressed carriers with odds ratios of 1.36 and 3.21 for the low and extremely low MBL genotypes, respectively (P = .01). The low-expression promoter haplotype XA (OR = 1.97) and the mutant haplotype YB (OR = 1.90) were also associated with the cirrhosis and hepatocellular carcinoma (P = .002). As expected, the lower serum MBL levels in progressed carriers as compared with nonprogressed carriers were due to an overrepresentation of low and extremely low MBL genotypes. Moreover, MBL could bind HBsAg in a dose- and calcium-dependent and mannan-inhibitable manner in vitro, suggesting that binding occurs via the carbohydrate recognition domains. This binding also enhanced C4 deposition. In conclusion, these results suggest that low MBL genotypes associate with the occurrence of cirrhosis and hepatocellular carcinoma in progressed HBsAg carriers, and MBL can bind HBsAg. Copyright © 2005 by the American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/76717
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChong, WPen_HK
dc.contributor.authorTo, YFen_HK
dc.contributor.authorIp, WKen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorPoon, TPen_HK
dc.contributor.authorWong, WHSen_HK
dc.contributor.authorLai, CLen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2010-09-06T07:24:11Z-
dc.date.available2010-09-06T07:24:11Z-
dc.date.issued2005en_HK
dc.identifier.citationHepatology, 2005, v. 42 n. 5, p. 1037-1045en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76717-
dc.description.abstractMannose binding lectin (MBL) is a pattern-recognition molecule of the innate immune system. The roles of MBL and its gene (mbl2) polymorphisms, - 221X/Y and codon 54A/B, in hepatitis B virus (HBV) infection were investigated in this study. We recruited 320 nonprogressed hepatitis B surface antigen (HBsAg) carriers; 199 progressed HBsAg carriers with hepatocellular carcinoma or cirrhosis; 87 spontaneously recovered individuals who were HBsAg negative and anti-HBs and anti HBc positive; and 484 controls who were naïve to HBV. There was no significant difference between nonprogressed carriers, spontaneously recovered individuals, and controls in terms of serum MBL levels and mbl2 polymorphisms distributions. However, the low MBL genotypes had a dose-dependent correlation with the cirrhosis and hepatocellular carcinoma in progressed carriers with odds ratios of 1.36 and 3.21 for the low and extremely low MBL genotypes, respectively (P = .01). The low-expression promoter haplotype XA (OR = 1.97) and the mutant haplotype YB (OR = 1.90) were also associated with the cirrhosis and hepatocellular carcinoma (P = .002). As expected, the lower serum MBL levels in progressed carriers as compared with nonprogressed carriers were due to an overrepresentation of low and extremely low MBL genotypes. Moreover, MBL could bind HBsAg in a dose- and calcium-dependent and mannan-inhibitable manner in vitro, suggesting that binding occurs via the carbohydrate recognition domains. This binding also enhanced C4 deposition. In conclusion, these results suggest that low MBL genotypes associate with the occurrence of cirrhosis and hepatocellular carcinoma in progressed HBsAg carriers, and MBL can bind HBsAg. Copyright © 2005 by the American Association for the Study of Liver Diseases.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshCodonen_HK
dc.subject.meshComplement C4 - metabolismen_HK
dc.subject.meshDisease Progressionen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenotypeen_HK
dc.subject.meshHepatitis B Surface Antigens - blood - metabolismen_HK
dc.subject.meshHepatitis B, Chronic - metabolism - physiopathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLiver Cirrhosis - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMannose-Binding Lectin - blood - genetics - metabolismen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPolymorphism, Geneticen_HK
dc.titleMannose-binding lectin in chronic hepatitis B virus infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=42&issue=5&spage=1037&epage=1045&date=2005&atitle=Mannose-binding+lectin+in+chronic+hepatitis+B+virus+infectionen_HK
dc.identifier.emailYuen, MF: mfyuen@hkucc.hku.hken_HK
dc.identifier.emailPoon, TP: poontp@hkucc.hku.hken_HK
dc.identifier.emailLai, CL: hrmelcl@hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hkucc.hku.hken_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityPoon, TP=rp00446en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/hep.20891en_HK
dc.identifier.pmid16231358-
dc.identifier.scopuseid_2-s2.0-30044438804en_HK
dc.identifier.hkuros112697en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-30044438804&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume42en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1037en_HK
dc.identifier.epage1045en_HK
dc.identifier.isiWOS:000232948100008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChong, WP=8634104400en_HK
dc.identifier.scopusauthoridTo, YF=11641177600en_HK
dc.identifier.scopusauthoridIp, WK=35991732900en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridPoon, TP=7103097223en_HK
dc.identifier.scopusauthoridWong, WHS=13310222200en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK

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