Interleukin-28 gene polymorphisms may contribute to HBsAg persistence and the development of HBeAg-negative chronic hepatitis B

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dc.contributor.authorKaratayli, Senem C.
dc.contributor.authorBozdayi, Mithat
dc.contributor.authorKaratayli, Ersin
dc.contributor.authorOzturk, Tugba
dc.contributor.authorHusseini, Abbas A.
dc.contributor.authorAlbayrak, Rabia
dc.contributor.authorOzkan, Muhip
dc.date.accessioned2024-04-24T17:11:47Z
dc.date.available2024-04-24T17:11:47Z
dc.date.issued2015
dc.departmentDicle Üniversitesien_US
dc.description.abstractBackground & AimsAim of this study was to investigate whether a potential association exists between several single nucleotide polymorphisms (SNPs) of the IL-28B gene (rs12979860, rs1188122, rs8099917, rs8105790, rs12980275) and HBsAg persistence. Further, a potential effect on the development of HBeAg-negative CHB vs. inactive HBsAg carrier state was assessed in a genotype D HBV cohort. A cohort of chronic HDV patients was also used to see if they behave differently compared to chronic HBV patients. MethodsThis study was conducted in three main patient cohorts: Group 1 consisted of 482 patients with HBsAg persistence. Of them 143 were inactive carriers, 94 had HBeAg-positive chronic hepatitis B (CHB) and 245 had anti-HBe-positive CHB. Group 2 represents spontaneously recovered HBV patients; they were anti-HBs and anti-HBc positive. Group 3 consisted of 176 chronic hepatitis delta (CHD) patients with antidelta and HDV-RNA positivity. DNA sequencing was performed for genotyping. ResultsWhen patients with HBsAg persistence were compared with spontaneously recovered patients, a significant difference was observed for rs8105790 (P<0.0001), rs12980275 (P<0.02). Patients who had the CC/TC genotype for rs8105790 (P<0.0001) and AA genotype for 1188122 (P<0.02) were more likely to be inactive HBsAg carriers, when inactive HBsAg carriers were compared with HBeAg-negative CHB patients. Comparison of CHD patients vs. recovered HBV patients was parallel to that of HBV persistence vs. recovered HBV with similar significant differences in same SNPs. ConclusionThese results suggest that IL-28B polymorphisms may contribute to HBsAg persistence and the development of the inactive HBsAg carrier state.en_US
dc.identifier.doi10.1111/liv.12595
dc.identifier.endpage853en_US
dc.identifier.issn1478-3223
dc.identifier.issn1478-3231
dc.identifier.issue3en_US
dc.identifier.pmid24840315
dc.identifier.scopus2-s2.0-84922710592
dc.identifier.scopusqualityQ1
dc.identifier.startpage846en_US
dc.identifier.urihttps://doi.org/10.1111/liv.12595
dc.identifier.urihttps://hdl.handle.net/11468/17724
dc.identifier.volume35en_US
dc.identifier.wosWOS:000349781900017
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofLiver International
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectHepatitis B Infectionen_US
dc.subjectHepatitis Delta Infectionen_US
dc.subjectInterferon Lambda 3en_US
dc.subjectInterleukin 28 Ben_US
dc.subjectSingle Nucleotide Polymorphismsen_US
dc.titleInterleukin-28 gene polymorphisms may contribute to HBsAg persistence and the development of HBeAg-negative chronic hepatitis Ben_US
dc.titleInterleukin-28 gene polymorphisms may contribute to HBsAg persistence and the development of HBeAg-negative chronic hepatitis B
dc.typeArticleen_US

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