Interleukin-28 gene polymorphisms may contribute to HBsAg persistence and the development of HBeAg-negative chronic hepatitis B
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Tarih
2015
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Wiley
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Background & 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.
Açıklama
Anahtar Kelimeler
Hepatitis B Infection, Hepatitis Delta Infection, Interferon Lambda 3, Interleukin 28 B, Single Nucleotide Polymorphisms
Kaynak
Liver International
WoS Q Değeri
Q1
Scopus Q Değeri
Q1
Cilt
35
Sayı
3
