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Article: Polymorphisms of type I interferon receptor 1 promoter and their effects on chronic hepatitis B virus infection

TitlePolymorphisms of type I interferon receptor 1 promoter and their effects on chronic hepatitis B virus infection
Authors
KeywordsChronic HBV infection
Haplotypes
IFNAR1 promoter polymorphisms
Transcriptional activity
Issue Date2007
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhep
Citation
Journal Of Hepatology, 2007, v. 46 n. 2, p. 198-205 How to Cite?
AbstractBackground/Aims: Exposure to HBV leads to a distinct clinical course which is partially pertained to host genetic variability. We aimed to study polymorphisms of type I interferon receptor 1 (IFNAR1) promoter and their potential effects on chronic HBV infection. Methods: Polymorphisms of IFNAR1 promoter were identified in 320 chronic hepatitis B patients, 148 spontaneously recovered individuals, 148 healthy Chinese donors and 114 Caucasians. Their functional capability in driving reporter gene expression was analyzed. Results: Four polymorphic alleles were identified at loci -568, -408, -77 and -3. Association analysis revealed that carriers of alleles -568G, -408C and their related haplotype I were less susceptible to chronic HBV infection whereas those of alleles -568C, -408T and related haplotype III were significantly associated with higher risk to chronic hepatitis B (P < 0.01). In a reporter-driven system, the promoter variants with alleles -408C and -3C could drive higher expression of the reporter gene than those with alleles -408T and -3T (P < 0.01). Interestingly, an allele with 9 GT repeats at -77 that was rarely found in Chinese but prevalent in Caucasian exhibited the highest transcriptional ability. Conclusions: Our results showed that polymorphisms of IFNAR1 promoter may affect, at least in part, the outcomes of HBV infection. © 2006 European Association for the Study of the Liver.
Persistent Identifierhttp://hdl.handle.net/10722/78745
ISSN
2014 Impact Factor: 11.336
2014 SCImago Journal Rankings: 3.477
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Jen_HK
dc.contributor.authorLu, Len_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorLam, TWen_HK
dc.contributor.authorChung, CPen_HK
dc.contributor.authorLam, CLen_HK
dc.contributor.authorZhang, Ben_HK
dc.contributor.authorWang, Sen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorWu, SHen_HK
dc.contributor.authorPoon, VKen_HK
dc.contributor.authorNg, Fen_HK
dc.contributor.authorChan, CCen_HK
dc.contributor.authorJiang, Sen_HK
dc.contributor.authorYuen, KYen_HK
dc.contributor.authorZheng, BJen_HK
dc.date.accessioned2010-09-06T07:46:16Z-
dc.date.available2010-09-06T07:46:16Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Hepatology, 2007, v. 46 n. 2, p. 198-205en_HK
dc.identifier.issn0168-8278en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78745-
dc.description.abstractBackground/Aims: Exposure to HBV leads to a distinct clinical course which is partially pertained to host genetic variability. We aimed to study polymorphisms of type I interferon receptor 1 (IFNAR1) promoter and their potential effects on chronic HBV infection. Methods: Polymorphisms of IFNAR1 promoter were identified in 320 chronic hepatitis B patients, 148 spontaneously recovered individuals, 148 healthy Chinese donors and 114 Caucasians. Their functional capability in driving reporter gene expression was analyzed. Results: Four polymorphic alleles were identified at loci -568, -408, -77 and -3. Association analysis revealed that carriers of alleles -568G, -408C and their related haplotype I were less susceptible to chronic HBV infection whereas those of alleles -568C, -408T and related haplotype III were significantly associated with higher risk to chronic hepatitis B (P < 0.01). In a reporter-driven system, the promoter variants with alleles -408C and -3C could drive higher expression of the reporter gene than those with alleles -408T and -3T (P < 0.01). Interestingly, an allele with 9 GT repeats at -77 that was rarely found in Chinese but prevalent in Caucasian exhibited the highest transcriptional ability. Conclusions: Our results showed that polymorphisms of IFNAR1 promoter may affect, at least in part, the outcomes of HBV infection. © 2006 European Association for the Study of the Liver.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhepen_HK
dc.relation.ispartofJournal of Hepatologyen_HK
dc.rightsJournal of Hepatology. Copyright © Elsevier BV.en_HK
dc.subjectChronic HBV infectionen_HK
dc.subjectHaplotypesen_HK
dc.subjectIFNAR1 promoter polymorphismsen_HK
dc.subjectTranscriptional activityen_HK
dc.subject.meshAsian Continental Ancestry Group - geneticsen_HK
dc.subject.meshConvalescenceen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshHaplotypesen_HK
dc.subject.meshHepatitis B, Chronic - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLinkage Disequilibriumen_HK
dc.subject.meshMaleen_HK
dc.subject.meshPolymorphism, Single Nucleotideen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshReceptor, Interferon alpha-beta - geneticsen_HK
dc.subject.meshTranscription, Geneticen_HK
dc.titlePolymorphisms of type I interferon receptor 1 promoter and their effects on chronic hepatitis B virus infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0168-8278&volume=46&issue=2&spage=198&epage=205&date=2007&atitle=Polymorphisms+of+type+I+interferon+receptor+1+promoter+and+their+effects+on+chronic+hepatitis+B+virus+infectionen_HK
dc.identifier.emailLu, L:liweilu@hkucc.hku.hken_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_HK
dc.identifier.emailZheng, BJ:bzheng@hkucc.hku.hken_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jhep.2006.08.017en_HK
dc.identifier.pmid17125879-
dc.identifier.scopuseid_2-s2.0-33845678522en_HK
dc.identifier.hkuros132963en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33845678522&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume46en_HK
dc.identifier.issue2en_HK
dc.identifier.spage198en_HK
dc.identifier.epage205en_HK
dc.identifier.isiWOS:000243813100004-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridZhou, J=7405550773en_HK
dc.identifier.scopusauthoridLu, L=7403963552en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridLam, TW=7202522868en_HK
dc.identifier.scopusauthoridChung, CP=19642564200en_HK
dc.identifier.scopusauthoridLam, CL=7402990922en_HK
dc.identifier.scopusauthoridZhang, B=35427050800en_HK
dc.identifier.scopusauthoridWang, S=8543927800en_HK
dc.identifier.scopusauthoridChen, Y=25927793500en_HK
dc.identifier.scopusauthoridWu, SH=14326090600en_HK
dc.identifier.scopusauthoridPoon, VK=6603703384en_HK
dc.identifier.scopusauthoridNg, F=7103125273en_HK
dc.identifier.scopusauthoridChan, CC=16021156900en_HK
dc.identifier.scopusauthoridJiang, S=7404453146en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK

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