The past 3 decades have witnessed remarkable advances in knowledge about viral hepatitis. We have moved from the belief, before the early 1970s, that only two vaguely defined viruses existed (infectious and serum; A and B) to the identification by the mid-1990s of six cloned hepatitis agents (A through E and G), with the likelihood that there are still others that await full characterization (GB, F ). Furthermore, we now have safe and effective vaccines that can provide prolonged protection from infection by the hepatitis A and B viruses. The global eradication of these infections is no longer a pipe dream; it is clearly a reachable goal. Because much of the recent virological progress has been achieved through the exploding technology of molecular biology, the gains that have drawn the greatest attention have come largely from detecting and characterizing "new" hepatitis agents. However, the rapidity with which these hepatitis viruses have been identified and specific serological assays have been developed has overwhelmed our capacity to fully characterize the spectrum of diseases they cause and their long-term consequences. This is particularly the case for the agents that have the potential to induce chronic hepatitis (hepatitis B, D, and c).
The advent of sophisticated and sensitive seroassays, developed through these recent advances, has uncovered the interesting and disturbing fact that acute and chronic hepatitis B and C, and to a lesser extent hepatitis D, may occur with few symptoms or signs of illness. Chronic hepatitis C, in particular, may exist in the total absence of evidence of clinical illness and even in the absence of biochemical markers of hepatitis. Several important issues can be derived from this discovery.
First, because chronic hepatitis B and C are largely asymptomatic entities, the true prevalences of these two viral diseases are not well established. Nevertheless, increasing numbers of recent but scattered surveys suggest that chronic hepatitis C is far more com-From the