Hepatitis C virus (HCV) is a major cause of chronic liver disease with about 170 million people infected worldwide. Up to 70% of patients will have persistent infection after inoculation, making this disease a significant cause of morbidity and mortality.
The severity of disease varies widely from asymptomatic chronic infection to cirrhosis and hepatocellular carcinoma. Since the discovery of HCV in 1989, the treatment of hepatitis C has considerably improved. Recently, combination of pegylated interferons with ribavirin gives a response rate of about 55%. Treatment is indicated in patients with moderate or severe necroinflammation or fibrosis. The tolerability of combination therapy is relatively poor with a frequent flu-like syndrome and an impaired quality of life.
In addition to viral and environmental behavioural factors, host genetic diversity is believed to contribute to the spectrum of clinical outcomes in HCV infection. The sequencing of the human genome, together with the development of high-throughput technologies that measure the function of the genome, have afforded unique opportunities to develop profiles that can distinguish, identify and classify discrete subsets of disease, predict the disease outcome or predict the response to therapy. This paper reviews the published literature on gene expression associated with the HCV infection (HCV infection, fibrosis progression), and also according to response to therapy.
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