Hepatitis B is caused by a DNA virus that is often parenterally transmitted. It causes typical symptoms of viral hepatitis, including anorexia, malaise, and jaundice. Fulminant hepatitis and death may occur. Chronic infection can lead to cirrhosis and/or hepatocellular carcinoma. Diagnosis is by serologic testing. Treatment is supportive. Vaccination is protective and postexposure use of hepatitis B immune globulin may prevent or attenuate clinical disease.
(See also Causes of Hepatitis, Overview of Acute Viral Hepatitis, and Chronic Hepatitis B.)
Hepatitis B virus (HBV) is the most thoroughly characterized and complex hepatitis virus. The infective particle consists of a viral core plus an outer surface coat. The core contains circular double-stranded DNA and DNA polymerase, and it replicates within the nuclei of infected hepatocytes. A surface coat is added in the cytoplasm and, for unknown reasons, is produced in great excess.
HBV is the 2nd most common cause of acute viral hepatitis after hepatitis A. Prior unrecognized infection is common but is much less widespread than that with hepatitis A virus. In the US, 3218 cases of acute hepatitis B infection were reported in 2016—a decrease from the 25,000 annual cases reported before use of hepatitis B vaccine became widespread. However, because many cases are not recognized or not reported, the Centers for Disease Control and Prevention (CDC) estimates that the actual number of new infections was about 20,900 in 2016 (1).
HBV, for unknown reasons, is sometimes associated with several primarily extrahepatic disorders, including polyarteritis nodosa, other connective tissue diseases, membranous glomerulonephritis, and essential mixed cryoglobulinemia. The pathogenic role of HBV in these disorders is unclear, but autoimmune mechanisms are suggested.
