
Association of tumor necrosis factor alpha -238G/A and -308G/A promotor polymorphisms with clearance of Hepatitis B virus infection in Turkish population
Author(s) -
Ahmet Çağkan İnkaya,
Emel Türk Arıbaş,
İbrahim Erayman,
Hasan Acar,
Bahar Kandemir,
Mehmet Bitirgen
Publication year - 2019
Publication title -
acta medica
Language(s) - English
Resource type - Journals
ISSN - 2147-9488
DOI - 10.32552/2019.actamedica.341
Subject(s) - medicine , immunology , hepatitis b virus , hepatitis b , immunity , population , turkish population , virology , virus , biology , genotype , immune system , gene , genetics , environmental health
Aim: 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.
Material and Methodology: 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 immunity groups, respectively. Frequencies of polymorphisms at positions -238 and -308 in the promotor of tumor necrosis factor alpha gene were not different between chronic hepatitis B and natural immunity groups.
Conclusion: 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.