Hepatitis B Virus as an Environmental Carcinogen

Abstract

Hepatitis B virus (HBV) is one of the most common and interesting human viruses. Investigation of HBV during the 1970s revealed unique antigenic, ultrastructural, molecular, and biological features which distinguished it from members of all of the recognized virus groups. One of the most notable features of this virus was its DNA structure. Virions contain small circular DNA molecules (1) that are partly single-stranded (2–4) and a DNA polymerase in the virion (5,6) can repair the DNA to make it fully double-stranded (2,3). Among the unique biological features are its liver tropism (7) and the common occurrence of persistent infection with viral antigen and infectious virus in high concentrations in the blood (8–11) continuously for years. This pattern of infection accounts for the transmission of HBV by percutaneous transfer of serum and serum-containing material. Several disease syndromes in addition to acute hepatitis may occur during acute and chronic HBV infection. Included are a serum sickness-like syndrome, membranous glomerulonephritis, and necrotizing vasculitis (polyarteritis), all probably related to viral antigen-antibody complex mediated tissue injury (12). In addition, persistent infection can be associated with a normal liver or with chronic hepatitis. The latter may be severe and progressive, and lead to cirrhosis and in some cases hepatocellular carcinoma (13). Its narrow host range (confined to man and a few higher primates) and failure so far to infect tissue culture cells have made it difficult to investigate some questions about HBV.