Infection with the Hepatitis C virus (HCV) affects nearly 200 million people in the world. It is a leading cause of
chronic hepatitis,
cirrhosis and
hepatocellular carcinoma (HCC). It is estimated that 25% of HCC worldwide is related to HCV, being the main cause in Western Europe, North America and Japan. HCV can be implicated in the development of HCC in an indirect way through induction of chronic
inflammation, or directly by means of
viral proteins activating several signaling pathways. For patients with clinically significant hepatic
fibrosis there is widespread agreement that
antiviral therapy is indicated in order to eliminate the virus. It is generally accepted that sustained virologic response (SVR), i.e. undetectable HCV
RNA at 24 weeks
after treatment withdrawal, is associated with resolution of
liver disease in patients without
cirrhosis. In the last decades, results of treatment for
chronic hepatitis C have improved substantially. The current standard of care is a combination of pegylated
interferon and
ribavirin for 24 to 48 weeks, depending on the genotype. In the near future, this standard of care will include addition of directly-acting
antivirals. In 2011 two
protease inhibitors (
boceprevir and
telaprevir) have been registered for use in adults with genotype 1
chronic hepatitis C, increasing the SVR rates from less than 50% to about 70% in patients treated with a triple combination. There is limited evidence for the role of
interferon-based
therapy in primary, secondary and tertiary prophylaxis of HCC in patients with
chronic Hepatitis C, as most studies were primarily designed to assess the
antiviral effect of treatment and not the long-term impact on the natural history of the disease. Further prospective studies using the more successful emerging treatments of
chronic hepatitis C are to be conducted to evaluate the risk of HCC.