Antiviral drug on hepatitis B virus genotypes and drug resistance genes

Hepatitis B virus (HBV) resistance is mainly due to the production of HBV resistance genes. This study investigated antivirus drug’s role in HBV resistance genes and genotypes. 200 HBV patients treated with lamivudine from January 2021 to December 2021 were enrolled. Peripheral blood samples were collected. HBV genotype and drug resistance gene mutation sites were analyzed. The alanine aminotransferase (ALT), aspartate aminotransferase (AST), ALT/AST ratios were analyzed. The serum HBV covalent circular closed DNA (cccDNA) load and HBV-DNA load were analyzed by fluorescence quantitative PCR (FQ-PCR). There were 72 cases of genotype B (36.0%, 72/200), 81 genotype C (40.5%, 81/200), and 47 genotype B + C (23.5%, 47/200). There were no differences in ALT, AST, ALT/AST ratio, HBV-DNA load, and serum HBV cccDNA load among the three genotypes (P > 0.05). After treatment, negative rate of hepatitis B E antibody (HBeAg), effective inhibition rate of HBV-DNA, and HBV cccDNA load decreased with no difference among three genotypes (P > 0.05). Major mutation sites of drug resistance genes were M204I/V/S, L180M, and A181V/T/S. After treatment, the positive rate of drug resistance locus mutation was increased (P < 0.05). There were three major mutation sites, including M204I/V/S, L180M and A181V/T/S, and genotypes B and C in HBeAg-positive HBV patients. The efficacy of lamivudine was not related to genotype, but could increase gene mutation rate.