Premium
Evaluation of IL10 , IL19 and IL20 gene polymorphisms and chronic hepatitis B infection outcome
Author(s) -
Truelove Ann L.,
Oleksyk Taras K.,
Shrestha Sadeep,
Thio Chloe L.,
Goedert James J.,
Donfield Sharyne M.,
Kirk Gregory D.,
Thomas David L.,
O’Brien Stephen J.,
Smith Michael W.
Publication year - 2008
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.2008.00770.x
Subject(s) - gene , outcome (game theory) , chronic hepatitis , interleukin 10 , genetics , biology , medicine , immunology , virus , mathematics , cytokine , mathematical economics
Summary Hepatitis B virus (HBV) infection remains a serious global health problem despite the availability of a highly effective vaccine. Approximately 5% of HBV‐infected adults develop chronic hepatitis B, which may result in liver cirrhosis or hepatocellular carcinoma. Variants of interleukin‐10 ( IL10 ) have been previously associated with chronic hepatitis B infection and progression to hepatocellular carcinoma. Single nucleotide polymorphisms (SNP; n = 42) from the IL10 , IL19 and IL20 gene regions were examined for an association with HBV infection outcome, either chronic or recovered, in a nested case–control study of African Americans and European Americans. Among African Americans, three nominally statistically significant SNP associations in IL10 , two in IL20 , and one haplotype association were observed with different HBV infection outcomes ( P = 0.005–0.04). A SNP (rs1518108) in IL20 deviated significantly from Hardy–Weinberg equilibrium in African Americans, with a large excess of heterozygotes in chronic HBV‐infected cases ( P = 0.0006), which suggests a strong genetic effect. Among European Americans, a nominally statistically significant SNP association in IL20 and an IL20 haplotype were associated with HBV recovery ( P = 0.01–0.04). These results suggest that IL10 and IL20 gene variants influence HBV infection outcome and encourage the pursuit of further studies of these cytokines in HBV pathogenesis.