Kao P.-C.JIA-FENG WUYEN-HSUAN NILin Y.-T.HUEY-LING CHENSANDY HUEY-JEN HSUHONG-YUAN HSUMEI-HWEI CHANG2021-01-042021-01-0420101478-3223https://www.scopus.com/inward/record.uri?eid=2-s2.0-79951508924&doi=10.1111%2fj.1478-3231.2010.02340.x&partnerID=40&md5=64fb5fbbafaccce41233ea060399b99ahttps://scholars.lib.ntu.edu.tw/handle/123456789/537010Background: This study aimed to investigate the roles of tumour necrosis factor-α (TNF-α) gene polymorphisms in the spontaneous clearance of HBsAg after a hepatitis B virus (HBV) infection. Methods: Polymorphisms in the TNF-α (-1031 T to C, -863 C to A, -857 C to T, -308 G to A and -238 G to A transition) gene were evaluated in 274 chronic HBV-infected patients and 194 patients with resolved HBV infection. The peripheral blood mononuclear cells (PBMC) isolated from 77 (28%) of the 274 chronic HBV-infected patients with negative HBeAg and positive antibody to HBeAg were stimulated with HBcAg. Data on TNF-α genotypes and phenotypes in subjects with/without the A allele at the TNF-α -863 promoter single nucleotide polymorphism (rs1800630) were compared. Results: The A allele in the -863 promoter region of the TNF-α gene was present in 154 (56.2%) chronic HBV-infected patients and 87 (44.8%) patients who recovered from HBV infection (odds ratio 1.58; P < 0.01). The TNF-α -863 A allele genotype predicted lower TNF-α production by PBMC after in vitro HBcAg stimulation (P < 0.02). Conclusions: The A allele at the -863 locus of the promoter region of the TNF-α gene predicts lower HBcAg inducible TNF-α secretion. It is also associated with chronicity of HBV infection. ? 2010 John Wiley & Sons A/S.[SDGs]SDG3alanine; cysteine; guanine; hepatitis B surface antigen; threonine; tumor necrosis factor alpha; adult; allele; article; cell isolation; controlled study; cytokine release; disease association; disease severity; female; gene locus; genotype; hepatitis B; human; in vitro study; major clinical study; male; peripheral blood mononuclear cell; phenotype; promoter region; single nucleotide polymorphism; stimulation; Adult; Biological Markers; Case-Control Studies; Cells, Cultured; Chi-Square Distribution; Female; Gene Frequency; Genetic Predisposition to Disease; Hepatitis B; Hepatitis B Surface Antigens; Hepatitis B, Chronic; Humans; Linkage Disequilibrium; Logistic Models; Male; Middle Aged; Odds Ratio; Phenotype; Polymorphism, Single Nucleotide; Promoter Regions, Genetic; Proportional Hazards Models; Remission, Spontaneous; Risk Assessment; Risk Factors; Taiwan; Tumor Necrosis Factor-alpha; Young Adultjournal article10.1111/j.1478-3231.2010.02340.x208255562-s2.0-79951508924