Abstract
The existence of non-A, non-B hepatitis was deduced in the mid-1970s when the new serologic tests for hepatitis B virus infection could not explain a substantial proportion of the cases of transfusion-associated hepatitis.1 Subsequent studies showed that non-A, non-B hepatitis was transmitted mainly by exposure to contaminated blood or blood products, but sporadic or community-acquired disease was also recognized.2 The acute infection was characterized as mild, but with persistent inflammatory activity as a potential long-term liability.3 Retrospective analyses were initially unable to confirm the projections of morbidity due to chronic non-A, non-B infection, emphasizing instead its relatively benign short-term prognosis. . . .