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The type of cell-mediated responses expressed at the early stages of HBV infection can influence the subsequent outcome of hepatitis B. Indeed, recovery is associated with efficient activation of mechanisms of the innate immunity, which seem to be responsible for the early inhibition of viral replication. A subsequent activation of HBV-specific T cells is probably crucial to complement the effect of the innate immunity and to allow complete control of virus replication. Moreover, control of infection cannot be achieved without rapid and efficient development of anti-envelope neutralizing antibody responses that are needed for elimination of free viral particles and inhibition of cell to cell spread of the virus. In patients with chronic hepatitis B, HBV-specific T cell responses are weak or undetectable in the peripheral blood and T cells are attracted into the infected liver where they are diluted among virus non-specific T and non-T cells that are the predominant cell population of the intrahepatic infiltrate. The high viral and antigen load may be the main responsible for the T cell hyporesponsiveness typical of chronic patients through exhaustion of T cell responses and expansion of T cells able to produce Th2 cytokines. HBV is a typical non-cytopathic virus that can induce tissue damage of variable severity by stimulating a protective immune response that can simultaneously cause damage and protection, by curing intracellular virus through the destruction of virus infected cells. Therefore, immune elimination of infected cells can lead to the termination o