Hepatitis C virus is a flavivirus with an RNA genome and is the most important cause of parenteral non-A, non-B hepa-titis (NANBH) worldwide. Prior to identification of the virus, it was known as NANBH to differentiate it from viral causes of nonalcoholic hepatitis. Most patients infected with HCV have chronic liver disease, which progresses to cirrhosis and hepatocellular carcinoma.
Hepatitis C virus is the only member of the genus Hepacivirus in the family Flaviviridae of RNA-containing virus. HCV appears to be closely related to hepatitis D and dengue and yellow fever virus. It resembles flavivirus in structure and organization, and hence has been classified as a new genus Hepacivirus in the family Flaviviridae. Hepatitis C virus shows following morpho-logical feartures:
It is a spherical, enveloped, 9.4 kb, single-stranded RNA virus with a diameter of 55 nm.
The genome is approximately 9500 base pairs that encode 10 structural and regulatory proteins. Structural proteins include the core and two envelope proteins, namely, E1 and E2. These two envelope proteins undergo variation dur-ing infection due to hypervariable regions within their genes.
The viruses are ether sensitive and acid sensitive.
These viruses like other flaviviruses replicate in the endoplas-mic reticulum of hepatocytes.
Hepatitis C virus shows a considerable degree of genomic variations. There are six major genotypes (genotypes 1–6) and numerous subtypes which differ in their worldwide distribu-tion. Molecular differences between these genotypes are rela-tively large with as little as 55% genetic sequence homology and more than 80 subtypes are described. This genetic variability is the main stumbling block against the effort to develop an anti-HCV vaccine.