Abstract

The human hepatitis B virus (HBV) is a member of the hepadnavirus family, which is compromised of DNA viruses that share structural and biological features. HBV infectivity is characterized by a marked hepatotropism, which is a prominent feature of hepadnaviruses. Although the majority of individuals infected with HBV resolve the primary infection and develop lasting immunity to subsequent infection, clinical studies have shown that 5–10% of individuals are chronically infected with the virus (Redeker, 1975). It has been estimated that there are over 250 million chronic HBV carriers worldwide (Rossner, 1992). A clinical consequence of chronic HBV infection is cirrhosis of the liver, which can lead to liver failure and death (Degroote et al., 1979). Furthermore, epidemiological studies have demonstrated that there is a strong association between hepatocellular carcinoma (HCC) and chronic HBV infection (Szmuness, 1978; Beasley et al., 1981). This association is supported by the following evidence: 1) there is a strong correlation in the geographical distribution of HCC and the occurence of chronic HBV infection, and 2) the hepatitis B surface antigen (HBsAg) is detected with a marked frequency in individuals with HCC. There is additional compelling evidence which correlates HBV with carcinogenesis.

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