In the acute phase of acute viral hepatitis high serum iron and serum ferritin levels were found in all patients. The normalisation of the serum ferritin concentration parallelled that of the serum glutamic pyruvic transaminase activity. However serum iron levels remained elevated for a long period of time. Chemical analysis of liver tissue showed a low total liver depot iron concentration during the first two weeks of the disease, indicating that the high serum iron levels are caused by iron liberation from disintegrated hepatocytes. Patients studied after two weeks showed higher liver iron concentrations, in particular the non-ferritin iron fraction, reflecting iron accumulation in the reticulo-endothelial system. Indeed, histological examination in the patients studied after two weeks showed sinusoidal lining cell siderosis in addition to "diffuse iron" in clusters lining cells which in electron microscopical studies proved to be macrophages. These cells showed a positive immunohistological reaction for ferritin protein. It is suggested that during acute viral hepatitis two mechanisms act together, i.e. changes in iron metabolism caused by damage of the main iron depot organ (specific liver pathology) and changes in iron metabolism common to all infectious processes.