1. Introduction Treatment of hepatitis B virus (HBV) infection aims to: suppress HBV replication prevent progression of liver fibrosis prevent cirrhosis prevent hepatic decompensation reduce hepatocellular carcinoma (HCC) risk reduce liver-related mortality prevent mother-to-child transmission where indicated control HBV-related extrahepatic disease achieve durable immune control ideally achieve HBsAg loss, the closest currently available endpoint to a functional cure The cen

1. Introduction HBV drug resistance is the ability of hepatitis B virus (HBV) variants carrying specific genetic substitutions to replicate despite exposure to an antiviral drug at concentrations that would normally suppress susceptible virus. It is primarily a consequence of: the high replication rate of HBV the error-prone nature of the viral polymerase/reverse transcriptase selection pressure exerted by antiviral therapy inadequate suppression of viral replication Drug res

1. Introduction HBV viral load refers to the quantity of hepatitis B virus (HBV) DNA present in a patient's blood, usually measured in serum or plasma. It is one of the most important quantitative parameters in the evaluation and management of chronic hepatitis B. The standard method is: Quantitative nucleic acid amplification testing (NAAT), usually real-time PCR. HBV viral load is generally reported as: IU/mL — International Units per millilitre It provides a direct measure