Ten years have elapsed since the identification of the viral agent (hepatitis C virus [HCV]) responsible for hepatitis C was first reported.¹ This remarkable achievement occurred after >20 years of intense effort by investigators worldwide following the observation that at least 1 additional viral agent, other than hepatitis A and hepatitis B, was the major cause of posttransfusion hepatitis.²

	BACKGROUND

Before the discovery of HCV, the term non-A, non-B hepatitis (NANB) was used to designate viral hepatitis for which there were no recognized serologic or virologic markers. Because most instances of NANB hepatitis were, in reality, hepatitis C, prospective studies and observations conducted in the 1970s and 1980s shed much light on the clinical features and natural history of HCV infection in adults. However, the discovery and characterization of the viral agent was a major leap forward and rapidly led to the development of assays to detect anti-HCV antibodies and more recently to the application of polymerase chain reaction assays that recognize minute amounts of circulating HCV genome (HCV-RNA). The development of these tests have made it possible to firmly establish a diagnosis of hepatitis C in the clinical setting and have led to a better understanding of the salient epidemiologic, clinical, biochemical, and histologic manifestations of HCV infection. In addition, they provide information essential for obtaining a more accurate assessment of the effects of both established and experimental therapeutic regimens on the course of infection. Moreover, the ability to screen potentially infectious materials, such as blood donated for transfusion, has had an important impact in preventing the spread of hepatitis C.

	THE VIRAL AGENT

HCV is an enveloped RNA virus with a genome that consists of ~10 000 nucleotides.³ The virus is a member of the flavivirus family, which also includes other parenterally spread viruses, such as yellow fever and dengue. At least 6 genotypes as . . . [Full Text of this Article]