Hepatitis C Virus (HCV) is a small enveloped positive sense single-stranded (ss) RNA virus. The genome consists of a single open reading frame that is 9600 nucleotide bases long. It is the only known member of the H Epacivirus genus in the family Flaviviridae. Sequence analysis of HCV isolates around the world has revealed the presence of six major genotypes, labeled 1 through 6, and subtypes, labeled a through r. Worldwide, about 200 million people (3% of the worldâs population) are infected with HCV, and 3 to 4 million people are newly infected each year with a global 170 million chronic carriers at risk of developing liver cirrhosis and/or liver cancer. Approximately 4.1 to 5.2 million people in the United States have chronic HCV infection. Hence, HCV infections account for a substantial proportion of liver diseases worldwide.
Current standard therapy is the combination of pegylated interferon-Î± (PEG-IFN-Î±), ribavirin (RBV), and protease inhibitors boceprevir and telaprevir (TVR) for patients with chronic HCV infection. This strategy results in a sustained virologic response (SVR) rate of 50%-80% in chronic hepatitis C (CHC) infected patients depending on the type of genotype [5-8]. However, many patients neither qualify nor can tolerate the standard therapy [9,10], especially those infected with HCV genotype 1, due to the genetic diversity of HCV genotypes and genetic variation in host factor Interleukin 2. Effect of Differentially Expressed MicroRNAs 602 and 323-5p on Hepatitis C Virus Genotype 1b Viral Load in Infected Liver Cells: Samina Noorali,
Muhammad Sheraz, Shaniqua S Tisdale, Stacey S Dallas, Lauren M Simons, Raquel S White and Verlie A Tisdale
Last date updated on June, 2014