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WHO estimates suggest that worldwide 150–200 million people are chronic carriers of HCV. Of these up to 30% will develop chronic liver inflammation and fibrosis and progress to cirrhosis or hepatocellular carcinoma (HCC) in the long term. New HCV infections are still occurring, and most HCV carriers are unaware of their status. Therefore incidences of HCV-induced liver disease and cancer are predicted to rise in the coming decade in spite of important recent progress in the development of direct antiviral agents. These new treatments appear to have greatly improved efficacies and safety profiles combined with a high genetic barrier and they are likely to introduce an era of interferon-free therapy in the near future.1 Virological cure in the form of a sustained virological response (SVR) is predicted to become attainable for most patients, including HCV carriers that were previously difficult to treat.1 A number of clinical studies have now shown that therapeutically obtained SVR improves inflammation and fibrosis, decreases the risk for end-stage liver disease and improves quality of life.2 However, in a minority of patients with SVR (up to 12%) fibrosis levels do not reverse and can even progress to cirrhosis.3 Furthermore, HCC can still occur in patients with SVR long periods after treatment and an advanced pretreatment fibrosis stage is considered as a risk factor.4 Obtaining a better understanding of the molecular biology underlying fibrosis in chronic hepatitis C thus remains an important issue, particularly as antifibrotic treatment is not yet available.
Fibrosis is the result of excessive accumulation of collagen-rich extracellular matrix (ECM), or scar tissue in response to hepatic injury, which will distort the architecture of the liver and lead to progressive loss of organ function in the long term.5 The predominant cell type responsible for deposition of the collagen-rich …