Hepatitis C Virus

In the 1970s and 1980s, serological tests developed for hepatitis A and B viruses (HAV, HBV) indicated that most transfusion-associated hepatitis was not caused by either HAV or HBV, and were therefore named non-A, non-B hepatitis (NANBH). After detection of the first NANBH-specific clone, the entire viral genome of the now termed hepatitis C virus (HCV) was sequenced, and based on its structural and functional organization, HCV was classified into the family of the Flaviviridae, where it forms its own genus ‘hepacivirus’ (Choo et al., 1989; Kuo et al., 1989). At least six major viral genotypes (1 to 6) have been identified (Simmonds et al., 2005). Viral genotypes have specific geographic distribution. The determination of the viral genotype is important for transmission studies, and has major therapeutic implications. Patients infected with genotype 1 have a significantly lower rate of response to antiviral therapy compared to other genotypes (Manns et al., 2007). Genotypes display differences in nucleotide sequences below 30–35%, and within a genotype genomes are allocated into different subtypes if their sequences differ by over 20–25%. Furthermore, viral isolate(s) present in an infected individual can mutate into quasi-species (Simmonds et al., 2005; Xu et al., 2008).