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
2011 Impact Factor: 9.264
2011 SCImago Journal Rankings: 0.765
DOIhttp://dx.doi.org/10.1016/j.jhep.2006.08.017
ISI Accession Number IDWOS:000243813100004
ReferencesReferences in Scopus
DC Field
Value
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
2011 Impact Factor: 9.264
2011 SCImago Journal Rankings: 0.765
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
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