The dominant role of non-A, non-B in the pathogenesis of post-transfusion hepatitis: a clinical assessment.

Although clinically recognized since the time of Hippocrates, viral hepatitis has been a continually enigmatic disease with each new insight raising the spectre of a new complexity. Despite remarkable advances in the past decade emanating from the discovery of the Australia antigen (Blumberg, Alter and Visnich, 1965) and its eventual linkage to viral hepatitis type B (Prince, 1968), there remain a multitude of unresolved issues regarding aetiology, routes ©f transmission, host-virus interactions, chronic carrier states, relationship to chronic liver disease and hepatocellular carcinoma, methods of propagation and modes of treatment. The jnest recent addition to this compendium of unknowns is the classification of an increasing number of viral hepatitis cases into the category 'non-A, non-B'. Despite the absence of a confirmed infectious particle or a specific diagnostic test, there is increasing circumstantial and direct evidence that the agent of non-A, non-B hepatitis is by far the major cause of transfusion-associated hepatitis and one of the leading causes of chronic hepatitis, particularly chronic active hepatitis. The remainder of this chapter will cite the evidence for the existence of a non A, non-B agent, document its relationship to post­ transfusion hepatitis, present the pattern of its clinical presentation, support its frequent relationship to chronic liver disease and demonstrate that it is due to a transmissible agent which, though presumed to be a virus, has not been established as such. Lastly, this review will attempt to present the current direction of research to better define this increasingly recognized disease entity.