Hepatitis C Virus

Abstract

Prior to the late 1980s, the problem of the etiology of non-A, non-B (NANB) hepatitis was completely blurred. In the early 1980s, the pioneering work of several groups had clearly demonstrated the viral nature of the disease by injecting blood of infected individuals into chimpanzees, hence permitting a number of interesting findings. However, all attempts to characterize the virus and to develop specific diagnostic tests had failed. Clinical and experimental observations had led to the postulation of the existence of at least two distinct viruses, while electron microscopy had suggested a variety of virus-like particles. Attention had eventually focused on a particle with dimensions and inactivation sensitivity similar to those of togaviruses. In this climate, the cloning in E. coli by Choo et al. (1) of the genome of a virus that in the subsequent few months was shown to represent the most common etiologic agent of posttransfusion and community-acquired (also defined as sporadic or cryptogenetic) NANB hepatitis signified an extremely important breakthrough as well as an innovative approach to the demonstration of viral agents. Most of the information discussed below stems from this breakthrough.