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Article: A regulatory polymorphism in interferon-γ receptor 1 promoter is associated with the susceptibility to chronic hepatitis B virus infection

TitleA regulatory polymorphism in interferon-γ receptor 1 promoter is associated with the susceptibility to chronic hepatitis B virus infection
Authors
KeywordsHBV infection
IFNGR1
Promoter activity
SNP
Transcription regulation
Issue Date2009
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00251/index.htm
Citation
Immunogenetics, 2009, v. 61 n. 6, p. 423-430 How to Cite?
AbstractThe antiviral cascade triggered by interferon-γ (IFN-γ) represents a vital event for eradicating hepatitis B virus (HBV) in experimental animals. IFN-γ signaling is mediated through the ligand binding to IFN-γ receptor 1 (IFNGR1). Control of IFNGR1 expression level is one of the mechanisms by which cells modulate the potency of IFN-γ signaling. In this study, we comprehensively investigated the single nucleotide polymorphisms (SNPs) in IFNGR1 gene and correlated their occurrence to susceptibility to HBV infection in a Chinese population. A total of 983 participants, including 361 chronic hepatitis B patients, 256 individuals who had spontaneously recovered from HBV infection, and 366 healthy control subjects, were enrolled in the study. Polymerase chain reaction-restriction fragment length polymorphism was used to identify seven SNPs (-611A/G, -56C/T, 40G/A, 95C/T, 130A/G, 20685A/G, 21227T/C) in IFNGR1 gene. We found that -56C and -56T allele were associated with viral clearance and viral persistence, respectively (P∈=∈0.014). In a reporter-driven assay, we validated that the promoter variant with -56C exhibited a higher transcription level than that with -56T in HepG2 cells in a cell-type-specific pattern. We conclude that a functional -56C/T SNP in IFNGR1 promoter is associated with the clinical outcome of HBV infection in this Chinese population. © 2009 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/147603
ISSN
2015 Impact Factor: 2.303
2015 SCImago Journal Rankings: 1.557
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong
Funding Information:

This work was supported in part by the University Development Fund of the University of Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Jen_HK
dc.contributor.authorChen, DQen_HK
dc.contributor.authorPoon, VKMen_HK
dc.contributor.authorZeng, Yen_HK
dc.contributor.authorNg, Fen_HK
dc.contributor.authorLu, Len_HK
dc.contributor.authorHuang, JDen_HK
dc.contributor.authorYuen, KYen_HK
dc.contributor.authorZheng, BJen_HK
dc.date.accessioned2012-05-29T06:04:54Z-
dc.date.available2012-05-29T06:04:54Z-
dc.date.issued2009en_HK
dc.identifier.citationImmunogenetics, 2009, v. 61 n. 6, p. 423-430en_HK
dc.identifier.issn0093-7711en_HK
dc.identifier.urihttp://hdl.handle.net/10722/147603-
dc.description.abstractThe antiviral cascade triggered by interferon-γ (IFN-γ) represents a vital event for eradicating hepatitis B virus (HBV) in experimental animals. IFN-γ signaling is mediated through the ligand binding to IFN-γ receptor 1 (IFNGR1). Control of IFNGR1 expression level is one of the mechanisms by which cells modulate the potency of IFN-γ signaling. In this study, we comprehensively investigated the single nucleotide polymorphisms (SNPs) in IFNGR1 gene and correlated their occurrence to susceptibility to HBV infection in a Chinese population. A total of 983 participants, including 361 chronic hepatitis B patients, 256 individuals who had spontaneously recovered from HBV infection, and 366 healthy control subjects, were enrolled in the study. Polymerase chain reaction-restriction fragment length polymorphism was used to identify seven SNPs (-611A/G, -56C/T, 40G/A, 95C/T, 130A/G, 20685A/G, 21227T/C) in IFNGR1 gene. We found that -56C and -56T allele were associated with viral clearance and viral persistence, respectively (P∈=∈0.014). In a reporter-driven assay, we validated that the promoter variant with -56C exhibited a higher transcription level than that with -56T in HepG2 cells in a cell-type-specific pattern. We conclude that a functional -56C/T SNP in IFNGR1 promoter is associated with the clinical outcome of HBV infection in this Chinese population. © 2009 Springer-Verlag.en_HK
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00251/index.htmen_HK
dc.relation.ispartofImmunogeneticsen_HK
dc.subjectHBV infectionen_HK
dc.subjectIFNGR1en_HK
dc.subjectPromoter activityen_HK
dc.subjectSNPen_HK
dc.subjectTranscription regulationen_HK
dc.subject.meshCell Lineen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshChi-Square Distributionen_US
dc.subject.meshGene Frequencyen_US
dc.subject.meshGenetic Predisposition To Diseaseen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHepatitis B, Chronic - Genetics - Virologyen_US
dc.subject.meshHumansen_US
dc.subject.meshLogistic Modelsen_US
dc.subject.meshLuciferases - Genetics - Metabolismen_US
dc.subject.meshLuminescent Measurementsen_US
dc.subject.meshOdds Ratioen_US
dc.subject.meshPolymorphism, Single Nucleotideen_US
dc.subject.meshPromoter Regions, Genetic - Geneticsen_US
dc.subject.meshReceptors, Interferon - Geneticsen_US
dc.subject.meshSequence Analysis, Dnaen_US
dc.subject.meshTransfectionen_US
dc.titleA regulatory polymorphism in interferon-γ receptor 1 promoter is associated with the susceptibility to chronic hepatitis B virus infectionen_HK
dc.typeArticleen_HK
dc.identifier.emailZhou, J:jiezhou@hku.hken_HK
dc.identifier.emailLu, L:liweilu@hkucc.hku.hken_HK
dc.identifier.emailHuang, JD:jdhuang@hkucc.hku.hken_HK
dc.identifier.emailYuen, KY:kyyuen@hkucc.hku.hken_HK
dc.identifier.emailZheng, BJ:bzheng@hkucc.hku.hken_HK
dc.identifier.emailPoon, KM: vincent.poonkm@gmail.com-
dc.identifier.emailNg, F: fng@HKUCC-COM.hku.hk-
dc.identifier.authorityZhou, J=rp01412en_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.identifier.authorityHuang, JD=rp00451en_HK
dc.identifier.authorityYuen, KY=rp00366en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s00251-009-0377-8en_HK
dc.identifier.pmid19488747-
dc.identifier.scopuseid_2-s2.0-67349184045en_HK
dc.identifier.hkuros156492-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67349184045&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume61en_HK
dc.identifier.issue6en_HK
dc.identifier.spage423en_HK
dc.identifier.epage430en_HK
dc.identifier.isiWOS:000266822700001-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridZhou, J=7405550443en_HK
dc.identifier.scopusauthoridChen, DQ=26634742000en_HK
dc.identifier.scopusauthoridPoon, VKM=6603703384en_HK
dc.identifier.scopusauthoridZeng, Y=36985939000en_HK
dc.identifier.scopusauthoridNg, F=7103125273en_HK
dc.identifier.scopusauthoridLu, L=7403963552en_HK
dc.identifier.scopusauthoridHuang, JD=8108660600en_HK
dc.identifier.scopusauthoridYuen, KY=36078079100en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.citeulike4760302-

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