Abstract
There are at least three different viruses responsible for the common varieties of hepatitis: the hepatitis A virus (HAV), the hepatitis B virus (HBV), and an unidentified virus or group of viruses called non-A, non-B (NANB). The symptoms and extent of liver injury produced in acute viral hepatitis vary from a mild, non-icteric, subclinical illness to acute icteric hepatitis, massive necrosis and hepatic failure. It is estimated that 5–10% of adults infected with HBV develop a chronic carrier state, manifested by the presence of the surface antigen (HBsAg) in the blood. The severity and variability of clinical and pathological forms of HB are related to the intensity and virulence of the infection and the quality and quantity of the immune response. Although a role for immune responses in the pathogenesis of hepatic injury is not conclusively proved, the data, such as the consistency of humoral and cellular responses, the presence of abnormal plasma immunoregulatory proteins (rosette inhibitory factor, RIF) (15,16,17), decreased suppressor cell activity (21), and the presence within the liver itself of potent immunosuppressive molecules, are compatible with explanations for recovery, acute and chronic injury, and the carrier state. Following inoculation or ingestion, the virus reaches the liver, where extensive virus replication occurs within the hepatocytes.
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Skarinsky, E., Rubin, E. (1984). The Morphologic Expression of Hepatitis B. In: Millman, I., Eisenstein, T.K., Blumberg, B.S. (eds) Hepatitis B. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0369-3_6
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