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For more than two decades prior to the discovery of the hepatitis C virus (HCV), posttransfusion non-A, non-B (NANB) hepatitis was thought to have a viral etiology. In 1989, the virus was finally identified through a unique application of molecular cloning techniques by investigators at the Centers for Disease Control, and the Chiron Corporation (1). In a reversal of the usual sequence of events, HCV was identified and defined before its existence was substantiated through tissue culture growth, electron microscopic observation, or serologic detection. Molecular cloning of HCV preceded the use of any of the conventional methods of viral identification and serologic detection then evolved from the blind immunoscreening of millions of clones with serum from a patient who had NANB hepatitis (2). The peptide expressed in a single reactive clone (5-1-1) served as the basis for the first Food and Drug Administration (FDA)-licensed diagnostic test for detection of antibodies to HCV (3). |
