Volume 14, Issue 7 , Pages e580-e585, July 2010
Tumor necrosis factor-α-308A allele may have a protective effect for chronic hepatitis B virus infection in Mongoloid populations☆
Summary
Objectives
Previous studies on the tumor necrosis factor-α (TNF-α)-308 gene promoter polymorphism in chronic hepatitis B virus (HBV) infection have reported conflicting results.
Methods
We carried out a meta-analysis of 21 studies in relation to the TNF-α-308 gene promoter, involving a total of 4230 chronic HBV infection cases and 2905 controls.
Results
The overall meta-analysis indicated that −308A heterozygotes (GA) had a significant 27% decreased risk of developing chronic hepatitis B (CHB) (odds ratio (OR) 0.73; 95% confidence interval (CI) 0.57–0.93; p
=
0.012). For −308A allele homozygotes (AA) and carriers (GA+AA), the pooled odd ratios both indicated a significantly decreased risk of CHB (OR 0.28; 95% CI 0.19–0.43; p
=
0.0001; and OR 0.70; 95% CI 0.55–0.89; p
=
0.004, respectively). In subgroup analyses by ethnicity, a significantly decreased risk was associated with −308 variant genotypes (GA and AA) in Mongoloid populations in all genetic models. However, no significant associations were found in Caucasoids. Moreover, in the subgroup analyses by control group, significantly decreased risk was associated with −308 variant genotypes (GA and AA) in the group of spontaneously recovered cases in all genetic models; however, no significant associations were found in the group of healthy cases.
Conclusions
The TNF-α-308A allele is a protective factor for chronic HBV infection, especially in Mongoloids.
Keywords: Tumor necrosis factor-α 308 gene, Polymorphism, Chronic hepatitis B, Case–control study, Meta-analysis
☆ Data in this article were presented in poster form at the Second Ditan International Conference on Infectious Diseases, Beijing, China, November 14–17, 2008 (published in Int J Infect Dis 2008;12:S62).
PII: S1201-9712(09)00344-0
doi:10.1016/j.ijid.2009.08.010
© 2009 International Society for Infectious Diseases. Published by Elsevier Inc. All rights reserved.
Volume 14, Issue 7 , Pages e580-e585, July 2010
