Comparison of Basal Core Promoter Region Mutation and Precore Mutation among Monoinfected Hepatitis B Virus and Coinfected Hepatitis B Virus with Human Immunodeficiency Virus Patients

This is the authors' abstract. We don't add key points for this paper.

OBJECTIVES: Hepatitis B virus (HBV) has a partially double-stranded circular deoxyribonucleic acid (DNA) that replicates through reverse transcription, producing an intermediate ribonucleic acid (RNA). This replication process has a high chance of error, leading to several mutations in the genome. According to several studies conducted worldwide, the classical basal core promoter (BCP) double mutation (A to T at nucleotide 1762 and G to A at nucleotide 1764) in the BCP region and the mutation in the precore (PC) region (G to A at nucleotide 1896) of HBV DNA have a strong correlation with advanced liver disease. The present study aims to compare the role of BCP and PC mutations among two groups of patients: monoinfected HBV (acute and chronic) and coinfected HBV-HIV patients. METHODOLOGY: Thirty cases from each group of monoinfected (acute = 15 and chronic = 15) and coinfected patients were subjected to BCP and PC mutation identification by PCR-RFLP, confirmed by sequencing. The prevalence of BCP and PC mutations between the two groups was then compared statistically. RESULTS: The BCP mutation among chronic HBV and HBV-HIV coinfected patients was 66.67 and 19.23%, respectively, while the PC mutation among chronic HBV and HBV-HIV patients was 8.34 and 23.07%, respectively. Both mutations were higher among hepatitis B e antigen (HBeAg)-negative subjects. HBV/D was the major genotype among the BCP and PC mutant subjects. CONCLUSION: The BCP mutants in our study had a high percentage of HBeAg negativity, low DNA levels, and mildly elevated ALT levels, mimicking inactive carriers. BCP mutants have a strong association with chronic liver diseases, so identifying chronic inactive HBV patients harboring the BCP mutant is necessary, and they require a close follow-up regimen.