Optimization of molecular methodology for the detection of Hepatitis B Virus precore/BCP mutations and analysis of the risk to develop cirrhosis in the center of Tunisia
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Keywords

Hepatitis B virus
Precore mutant
Core-promoter mutant
Cirrhosis

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How to Cite

FODHA, I. ., RIANI, M. ., KACEM, S. ., BEN HAJ FREDJ, M. ., KETATA, S. ., LETAIEF, A. ., AJMI, S. ., BOUJAAFAR, N. ., & TRABELSI, A. . (2024). Optimization of molecular methodology for the detection of Hepatitis B Virus precore/BCP mutations and analysis of the risk to develop cirrhosis in the center of Tunisia. Revue Tunisienne De BIOLOGIE CLINIQUE, (24), 25–32. https://doi.org/10.71699/revtunbiolclin.vi24.64

Abstract

Chronic hepatitis B virus infections are the major cause of hepatocellular carcinoma worldwide. Progression of liver disease seems to be adversely affected by viral strain characteristics, such as genotype, precore and basal core promoter (BCP) mutation. The aims of the present study were the optimization of molecular methodology for the detection of Hepatitis B Virus precore/BCP mutations and thereafter the comparison in frequency of detection of such mutations between asymptomatic carriers and chronic Hepatitis B Virus infected patients with cirrhosis. Thirty-six Tunisian patients with chronic Hepatitis B Virus infection were investigated : 18 were asymptomatic carriers and 18 presented with cirrhosis. Precore and core-promoter mutations were detected using PCR (Polymerase Chain Reaction)-RFLP (Restriction Fragment Length Polymorphism) and PCR-sequencing methodology. The comparison between asymptomatic carriers and patients with cirrhosis showed a higher prevalence of precore (100% Vs 83%) and core-promoter mutations (44.4% vs 33.3%) in patients with cirrhosis. Nevertheless, these differences remained not significant statistically. The pathogenesis of hepatitis B infections is not completely understood. The present study supports the idea that patients with precore and BCP mutations seem to carry an increased risk for developing cirrhosis and hepatocellular carcinoma independently of viral load. Further studies are needed to definitely elucidate such a hypothesis.

https://doi.org/10.71699/revtunbiolclin.vi24.64
PDF (Français (France))
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