ArticleMolecular genetics & genomic medicine2019
TNF-α polymorphisms affect persistence and progression of HBV infection.
Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- miR-194-5p targets SOCS2 to predict pegIFNα treatment response in HBeAg-positive chronic hepatitis B patients.Virology journal · 2026Article
- Host and Viral Factors Influencing Chronic Hepatitis B Infection Across Three Generations in a Family.Current microbiology · 2024Article
- Associations between single nucleotide polymorphisms of cytokines and hepatitis B virus-related liver cirrhosis: A case-control study.Immunity, inflammation and disease · 2024Article
- Multifunctional roles of inflammation and its causative factors in primary liver cancer: A literature review.World journal of hepatology · 2023Review
- The hepatitis B virus pre-core protein p22 suppresses TNFα-induced apoptosis by regulating the NF-κB pathway.American journal of translational research · 2023Article
- Host Factors in the Natural History of Chronic Hepatitis B: Role of Genetic Determinants.International journal of hepatology · 2022Article
- CCL19 enhances CD8Journal of gastroenterology · 2021Article
- Article
- TNF-α polymorphisms affect persistence and progression of HBV infection.Molecular genetics & genomic medicine · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatitis B virus (HBV) infections are a major threat worldwide. Disease progression and outcome is diverse and depends on host genetic background. Recently, a high rate of HBV reactivation in individuals receiving tumor necrosis factor-α (TNF-α) antagonists showed the importance of this cytokine in HBV infection control. Here, we investigated the influence of TNF-α promoter polymorphisms on susceptibility to chronic HBV infection (CHB), liver injury progression and outcomes.
methodsA total of 231 patients with CHB constituted the study group and 100 healthy volunteers-the local control group. TNF-α -1031T/C, -863C/A, -857C/T, -308G/A, and -238G/A were genotyped using MALDI-TOF mass spectrometry.
resultsTNF-α -1031C and -863A alleles were observed more frequently in CHB group than in healthy controls. Carriers of TNF-α -1031C and -863A variant alleles had lower baseline levels of serum HBV DNA and lower liver necroinflammatory activity than dominant homozygotes. A -857CT genotype predisposed to higher necroinflammatory activity. No associations between TNF-α variants and liver fibrosis were found.
conclusionThis study indicates that TNF-α -863A and -1031C alleles are associated with increased susceptibility to CHB in individuals from northern Poland. The same variants determine the course of CHB, lowering viremia and reducing necroinflammatory activity of the liver.
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