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Hepatitis B virus (HBV) infection can cause acute, fulminant or chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). Perinatally or childhood acquired HBV infection usually causes subclinical or anicteric acute hepatitis and is associated with a high risk of chronicity (30 to 90 % of cases), whereas adult acquired infection may cause acute symptomatic hepatitis (approximately 30 % of patients) and is associated with a low risk of chronicity (less than 5%). Fulminant hepatic failure is unusual (0.1 to 0.5 % of patients), but acute coinfection with other hepatitis viruses increases the risk of fulminant hepatitis. Chronic HBV infection is a dynamic process with an early replicative phase and active liver disease and a late low or non replicative phase with remission of liver disease. Perinatally acquired HBV infection is characterized by a prolonged “immunotolerant ” phase with hepatitis B e antigen (HBeAg) positivity, high levels of serum HBV-DNA, normal levels of aminotransferases, minimal liver damage and very low rates of spontaneous HBeAg clearance. Patients with childhood or adult acquired infection and chronic hepatitis B usually present in the “immunoactive ” phase with elevated aminotransferases and liver necroinflammation at histology (HBeAg positive chronic hepatitis) and approximately 50 % will clear HBeAg within 5 years. The rate of spontaneous HBeAg seroconversion may vary in relation to the degree of the elevation of aminotransferases. Seroconversion from HBeAg to antibody to HBeAg marks the transition from chronic hepatitis to the inactiv