Abstract

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.

Highlights

  • Hepatitis B virus (HBV) is estimated to have infect- infancy results CHB in 90% patients whereas infeced more than 2 billion people worldwide, of whom, tion during adulthood leads to chronic infection in 400 million are chronically infected today and are at less than 5% of patients [5]

  • About early intrahepatic events in human infection, Outcome of HBV infection is affected by viral and data from the animal models of acute HBV infection host factors

  • These findings suggest that TNFα activity is crucial to control HBV infection and vi- Diseases ral replication

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Summary

INTRODUCTION

Hepatitis B virus (HBV) is estimated to have infect- infancy results CHB in 90% patients whereas infeced more than 2 billion people worldwide, of whom, tion during adulthood leads to chronic infection in 400 million are chronically infected today and are at less than 5% of patients [5]. TNFα kills HBx sensitized cells consuming alcohol 40g/day, patients with cirrhosis via apoptosis [10] and inhibits HBV core promot- and autoimmune hepatitis were excluded. These findings suggest that TNFα activity is crucial to control HBV infection and vi- Diseases ral replication. Genomic clear cells of liver recipients with -308AA allel, when DNA was isolated from peripheral blood leucochallenged with Con-A, produces TNFα thrice the cytes using standard phenol-chloroform methpatients with GG allele [16]. The aim of the present (Fermentas, England), 50 ng genomic DNA, 20 μL study was to determine whether certain TNF pro- 10 x buffer, and 1.5 mmol/L MgCl2, 1.2 μL primers motor polymorphisms affect outcome of HBV infec- and 10 pmol/L dNTPs. The PCR cycles were as foltion in Turkish population.

DNA fragments then identified by ultraviolet light
RESULTS
Findings
Genotype GG GA AA G A GG GA AA G A
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