A whole spectrum of consequence of viral hepatitis injury implicates directly a modulated antigenic profile expression that further modifies quantitatively the immune response to the infection.  It is in terms of such consequence that cytopathic injury and cytotoxicity as induced by T lymphocytes induce an ongoing injury to hepatocytes. Persistence of injury is itself another parameter of activity in accounting for transformation of the expression profile of infected hepatocytes.  The immune response would be sustained in the presence of persistent viral DNA in serum and tissues and in further allowing for transformation. The infected hepatocyte is indeed an expression consequence of injury that is precipitated by viral infection and driven by changing antigenic profile reactivity of the liver cells.  The cytotoxic T lymphocytes would transcend aspects of targeting or pooling dynamics within the liver but would promote consequences of injury as quantitatively predetermined immunologic response in perinatal or adult studies. Derived consequence of hepatocyte injury ranges from clearance of virus to acute and chronic hepatitis to a persistent state of antigenicity that perhaps may culminate in hepatocellular carcinogenesis.