| Alpha interferon was licensed for hepatitis B in 1992. In the past several years its use has been eclipsed by nucleoside analogue therapy; however, evidence suggests that it continues to bear promise as a treatment for hepatitis B, either alone or in combination with nucleoside analogue therapy. From a theoretical perspective, the different mechanisms of action of interferon and nucleoside analogues should make them complementary to each other. Furthermore, there has been a recent resurgence of interest in interferon with the development of the more potent and longer-acting pegylated forms. Figure 1 illustrates the life cycle of the hepatitis B virus (HBV).1 The dark and white circles indicate the mechanisms of action of interferon and nucleoside analogues, respectively. Interferon activates intracellular enzymes such as 2`5 oligoadenylate synthetase, resulting in the degradation of HBV mRNA; it also bolsters the cell-mediated immune response to HBV by augmenting expression of HLA class I antigen-presenting molecules on the surfaces of infected hepatocytes. The immunologically relevant viral peptides are located in a peptide-binding cleft on the HLA molecule. In contrast, nucleoside analogues competitively inhibit HBV DNA polymerase, interfering with the synthesis of the first and/or second HBV DNA strand http://www.freewebs.com/masaearning/medical.htm
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