PIP: Adults with a healthy immune system who are exposed to hepatitis B virus (HBV) usually suffer from a mild acute infection. The likelihood of chronicity is only 5%, but climbs as high as 90% in newborns and n the immunocompromised. Acute HBV infection can cause fulminant liver failure (case fatality rate of 80%). People with chronic infection tend to have no symptoms, normal liver enzymes, and normal or almost normal liver histology, making diagnosis difficult. Active viral replication occurs in most people with active liver disease. People with persistent active replication are at higher risk of death from liver disease or hepatocellular carcinoma (HCC) than those with inactive disease. HBV transmission occurs via sexual intercourse or blood or needle contact. In the US, iv drug use is the major risk factor for HBV infection in adults. Prevention of HBV infection is through patient education and vaccination. Some people advocate universal HBV vaccination because it is often difficult to vaccinate high risk populations and to identify risk factors. Universal vaccination is not cost effective in low risk areas, however, e.g., the US and Europe. Treatment for chronic HBV infection is limited. Response to interferon therapy depends on low HBV DNA levels, high transaminase levels, and a history of acute hepatitis. Short- and longterm response rates tend to be low, however ( 40% short term and much lower for longterm). Experimental drugs are thymosin and nucleoside analogues. Standard treatment for patients with end-stage chronic liver disease or fulminant hepatic failure is liver transplantation. High dose immune globulin is the best means to delay and prevent recurrent HBV infection in transplantation patients. Some problems with management of chronic HBV are prevention of HCC and recurrent HBV after transplantation. Variant viruses are mutations of the precore or of a surface gene. HIV/AIDS is often associated with HBV and hepatitis delta virus infection.