Journals / Acta Medica / 2019 / Cilt: 50 - Sayı: 1

Association of Tumor Necrosis Factor Alpha -238G/A and -308G/A Promotor Polymorphisms with Clearance of Hepatitis B Virus Infection in Turkish Population

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1–6
DOI
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⚡ TL;DR(Too Long; Didn't Read)

Thus, further studies needed to identify genetic predisposition to chronic hepatitis B infection.

📌 3 Key Takeaways

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Objective & Hypothesis:Objectives: Acute viral hepatitis B may lead to chronic hepatitis in 6% of adult population.
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Key Findings & Data:Materials and Methods: Chronic hepatitis B patients and age matched control cases with natural immunity to hepatitis B virus were recruited 1:1 in this study.
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Conclusion & Impact:Thus, further studies needed to identify genetic predisposition to chronic hepatitis B infection.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Objectives: Acute viral hepatitis B may lead to chronic hepatitis in 6% of adult population. We compared the frequency of Tumor necrosis factor alpha promotor polymorphisms in chronic hepatitis B patients and people with natural immunity against hepatitis B. Materials and Methods: Chronic hepatitis B patients and age matched control cases with natural immunity to hepatitis B virus were recruited 1:1 in this study. Tumor necrosis factor alpha -238G/A and -308G/A polymorphisms were studied with PCR-RFLP. χ2 test was performed in statistical analysis. Results: A total of 101 volunteers enrolled in two study groups. Thirty-eight men and 12 women constituted the chronic hepatitis B patient group and 40 men and 11 women recruited in natural immunity group. Frequency of -238G allele was 87.5% and 97% in chronic hepatitis B and natural immunity groups, respectively. Frequency of -308G allel was 93% and 92.1% in chronic hepatitis B and natural im- munity groups, respectively. Frequencies of polymorphisms at positions -238 and -308 in the promotor of tumor necrosis factor alpha gene were not different be- tween chronic hepatitis B and natural immunity groups. Discussion: Tumor necrosis factor alpha promoter polymorphisms at -238 and -308 positions do not effect the outcome hepatitis B infection in Turkish population. Clearance of hepatitis B virus infection is multifactorial. Thus, further studies needed to identify genetic predisposition to chronic hepatitis B infection.

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Cite This Article

İNKAYA, A. Ç., ARIBAŞ, E. T., ERAYMAN, İ., KANDEMİR, B., ACAR, H., BİTİRGEN, M. (2019). Association of Tumor Necrosis Factor Alpha -238G/A and -308G/A Promotor Polymorphisms with Clearance of Hepatitis B Virus Infection in Turkish Population. Acta Medica, Cilt: 50 - Sayı: 1, 1–6. https://ajindex.com/articles/141980

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References (14)

  1. Lavanchy D. Hepatitis B virus epidemiology, disease burden, treatment, and current and emerging prevention and control measures. J Viral Hepat 2004; 11: 97-107. World Health Organization Hepatitis B Fact Sheet No. 204 (Revised October 2000) https://www.who.int/en/news-room/ fact-sheets/detail/hepatitis-a (accessed in July 2018).
  2. Visvanathan K, Lewin SR Immunopathogenesis: Role of Innate and Adaptive Immune Reponses, Semin Liver Dis 2006; 26: 104-15.
  3. Thursz MR, Thomas HC. Pathogenesis of chronic hepatitis B. In: Thomas HC, Lemon S, Zuckermann A (Eds). Viral Hepatitis. Massachusetts; Blackwell Publishing Ltd, 2005; 308-22.
  4. De Franchis R, Hadengue A, Lau G, et al. EASL International Consensus Conference on Hepatitis B. 13-14 September, 2002
  5. Geneva, Switzerland. Consensus statement (long version). J Hepatol 2003; 39(suppl 1): S3-25. Murray JM, Wieland SF, Purcell RH et al. Dynamics of hepatitis B virus clearance in chimpanzees. Proc Natl Acad Sci USA 2005; 102: 17780–85.
  6. Guidotti LG, Rochford R, Chung J et al. Viral clearance without destruction of infected cells during acute HBV infection. Science 1999; 284: 825–29.
  7. Herbein G, O’Brien WA. Tumor Necrosis Factor (TNF)-α and TNF Receptors in Viral Pathogenesis, PSEBM 2000; 223: 241-57.
  8. Fang JW, Shen WW, Meager A, et al. Activation of the tumor necrosis factor-α system in the liver in chronic hepatitis B virus infection. Am J Gastroenterol 1996; 91:748-53.
  9. Su F, Schneider RJ. Hepatitis B virus x protein sensitizes cells to apoptotic killing by tumor necrosis factor-α. Proc Natl Acad Sci USA 1997; 94: 8744-49.
  10. Romero R, Lavine JE. Cytokine inhibiton of hepatitis B core pro- motor. Hepatology 1996; 23: 17-23.
  11. Tsui L V, Guidotti L G, Ishikawa T, et al. Posttranscriptional clear- ance of hepatitis B virus RNA by cytotoxic T lymphocyte-activat- ed hepatocytes. Proc Natl Acad Sci USA 1995; 92: 12398–402.
  12. Esteve M, Saro C, Gonzalez-Huix F, et al. Chronic hepatitis B reactivation following infliximab therapy in Crohn’s disease patients:need for primary prophylaxis. Gut 2004; 53: 1363–65. D’Alfonso S, Richiardi PM. A polymorphic variation in a putative regulation box of the TNFA promoter region. Immunogenetics 1994; 39: 150–54.
  13. Louis E, Franchimont D, Piron A, et al. Tumour necrosis factor (TNF) gene polymorphism influences TNF-alpha production in lipopolysaccharide (LPS)-stimulated whole blood cell culture in healthy humans. Clin Exp Immunol 1998; 113: 401–06.
  14. Fernandes H, Koneru B, Fernandes N et al. Investigation of pr