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Article: Polymorphisms of type I interferon receptor 1 promoter and their effects on chronic hepatitis B virus infection
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TitlePolymorphisms of type I interferon receptor 1 promoter and their effects on chronic hepatitis B virus infection
 
AuthorsZhou, J2
Lu, L2
Yuen, MF2
Lam, TW3
Chung, CP3
Lam, CL3
Zhang, B1
Wang, S1
Chen, Y5
Wu, SH2
Poon, VK2
Ng, F2
Chan, CC2
Jiang, S4
Yuen, KY2
Zheng, BJ2
 
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
 
CitationJournal Of Hepatology, 2007, v. 46 n. 2, p. 198-205 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.jhep.2006.08.017
 
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.
 
ISSN0168-8278
2013 Impact Factor: 10.401
 
DOIhttp://dx.doi.org/10.1016/j.jhep.2006.08.017
 
ISI Accession Number IDWOS:000243813100004
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZhou, J
 
dc.contributor.authorLu, L
 
dc.contributor.authorYuen, MF
 
dc.contributor.authorLam, TW
 
dc.contributor.authorChung, CP
 
dc.contributor.authorLam, CL
 
dc.contributor.authorZhang, B
 
dc.contributor.authorWang, S
 
dc.contributor.authorChen, Y
 
dc.contributor.authorWu, SH
 
dc.contributor.authorPoon, VK
 
dc.contributor.authorNg, F
 
dc.contributor.authorChan, CC
 
dc.contributor.authorJiang, S
 
dc.contributor.authorYuen, KY
 
dc.contributor.authorZheng, BJ
 
dc.date.accessioned2010-09-06T07:46:16Z
 
dc.date.available2010-09-06T07:46:16Z
 
dc.date.issued2007
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Hepatology, 2007, v. 46 n. 2, p. 198-205 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.jhep.2006.08.017
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.jhep.2006.08.017
 
dc.identifier.epage205
 
dc.identifier.hkuros132963
 
dc.identifier.isiWOS:000243813100004
 
dc.identifier.issn0168-8278
2013 Impact Factor: 10.401
 
dc.identifier.issue2
 
dc.identifier.openurl
 
dc.identifier.pmid17125879
 
dc.identifier.scopuseid_2-s2.0-33845678522
 
dc.identifier.spage198
 
dc.identifier.urihttp://hdl.handle.net/10722/78745
 
dc.identifier.volume46
 
dc.languageeng
 
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhep
 
dc.publisher.placeNetherlands
 
dc.relation.ispartofJournal of Hepatology
 
dc.relation.referencesReferences in Scopus
 
dc.rightsJournal of Hepatology. Copyright © Elsevier BV.
 
dc.subject.meshAsian Continental Ancestry Group - genetics
 
dc.subject.meshConvalescence
 
dc.subject.meshFemale
 
dc.subject.meshGenetic Predisposition to Disease
 
dc.subject.meshHaplotypes
 
dc.subject.meshHepatitis B, Chronic - genetics
 
dc.subject.meshHumans
 
dc.subject.meshLinkage Disequilibrium
 
dc.subject.meshMale
 
dc.subject.meshPolymorphism, Single Nucleotide
 
dc.subject.meshPromoter Regions, Genetic - genetics
 
dc.subject.meshReceptor, Interferon alpha-beta - genetics
 
dc.subject.meshTranscription, Genetic
 
dc.subjectChronic HBV infection
 
dc.subjectHaplotypes
 
dc.subjectIFNAR1 promoter polymorphisms
 
dc.subjectTranscriptional activity
 
dc.titlePolymorphisms of type I interferon receptor 1 promoter and their effects on chronic hepatitis B virus infection
 
dc.typeArticle
 
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Author Affiliations
  1. Donghu Hospital
  2. The University of Hong Kong
  3. Queen Elizabeth Hospital Hong Kong
  4. New York Blood Center
  5. Capital Medical University China