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肿瘤坏死因子-α-238A 等位基因增加了欧洲人群慢性乙型肝炎病毒感染的风险。

The tumour necrosis factor-α-238A allele increases the risk of chronic HBV infection in European populations.

机构信息

Department of Infection and Liver Diseases, Liver Research Center, The First Affiliated Hospital of Wenzhou Medical College, Wenzhou, China.

出版信息

J Viral Hepat. 2012 Feb;19(2):e11-7. doi: 10.1111/j.1365-2893.2011.01491.x. Epub 2011 Jul 22.

DOI:10.1111/j.1365-2893.2011.01491.x
PMID:22239507
Abstract

Tumour necrosis factor-α (TNF-α) plays a pivotal role in viral clearance and host immune response to hepatitis B virus (HBV) infection, of which the production capacity in individuals is demonstrated to be influenced by a single nucleotide polymorphism within the promoter region of TNF-α genes. However, there have been conflicting results reported in previous studies on TNF-α-238 and TNF-α-863 gene promoter polymorphisms in chronic HBV infection. To derive a more precise estimation of their relationship, we searched Pubmed (January, 1966-August, 2010) and China Biological Medicine Database (January, 1978-August, 2010) and carried out a meta-analysis involving nineteen studies that included 5245 chronic HBV infection cases and 3181 controls describing G238A genotypes, and eleven studies totalling 3576 cases and 2044 controls describing C863A genotypes. The overall meta-analysis did not suggest significant associations of TNF-α-238 and TNF-α-863 gene promoter polymorphisms with chronic HBV infection. However, in subgroup analysis by ethnicity, it indicated that TNF-α-238A allele carriers (GA + AA) in European populations had an increased risk of developing chronic HBV infection (OR = 2.22, 95% CI: 1.07-4.58, P = 0.032; OR = 4.46, 95% CI: 1.75-11.38, P = 0.002, respectively), when compared with spontaneous recovered and healthy populations, respectively. However, no significant associations were found in Asian populations in all genetic models. So, we draw the conclusion that the TNF-α-238A allele may increase the risk of chronic HBV infection in European populations.

摘要

肿瘤坏死因子-α(TNF-α)在清除病毒和宿主对乙型肝炎病毒(HBV)感染的免疫反应中起着关键作用,个体的产生能力被证明受到 TNF-α基因启动子区域内的单核苷酸多态性的影响。然而,在慢性 HBV 感染中 TNF-α-238 和 TNF-α-863 基因启动子多态性的先前研究中,报告了相互矛盾的结果。为了更准确地评估它们之间的关系,我们检索了 Pubmed(1966 年 1 月至 2010 年 8 月)和中国生物医学文献数据库(1978 年 1 月至 2010 年 8 月),并进行了荟萃分析,其中包括 19 项研究,共 5245 例慢性 HBV 感染病例和 3181 例对照,描述了 G238A 基因型,以及 11 项研究共 3576 例病例和 2044 例对照,描述了 C863A 基因型。总体荟萃分析表明,TNF-α-238 和 TNF-α-863 基因启动子多态性与慢性 HBV 感染之间没有显著关联。然而,按种族进行亚组分析表明,欧洲人群中 TNF-α-238A 等位基因携带者(GA + AA)发生慢性 HBV 感染的风险增加(OR = 2.22,95%CI:1.07-4.58,P = 0.032;OR = 4.46,95%CI:1.75-11.38,P = 0.002),与自发恢复和健康人群相比。然而,在所有遗传模型中,亚洲人群均未发现显著相关性。因此,我们得出结论,TNF-α-238A 等位基因可能增加欧洲人群慢性 HBV 感染的风险。

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