Molecular bases of hepatic fibrogenesis - genetic and therapeutical implications in chronic viral C hepatitis.

Hepatitis C virus represents one of the major health problems of actual world, as almost 170 million of world population and 1 million persons in Romania are infected with HCV. Considering the increasing importance of HCV, it is imposed that we elucidate the molecular mechanisms, which are the base of hepatic fibrogenesis and potential targets for therapy, for diminishing progression to cirrhosis and avoid the appearance of complications. Activation of stellate cells is the main event in hepatic fibrosis. They also express almost all key components needed for the pathological degradation of matrix and that is why they play an important role not only in the production, but also in the degradation of the matrix. Recently, the worldwide research has also been oriented towards another type of cells with possible function in fibrogenesis and response to antiviral therapy: hepatic progenitor cells. The presence of hepatic progenitor cells in chronic C viral hepatitis is associated with severity of the disease, grade of fibrosis and the risk of hepatocarcinoma. Traditionally perceived as irreversible, reversibility of advanced fibrosis has been described recently in antiviral therapy trials for chronic C viral hepatitis. The favorable effect of interferon therapy on hepatic histology, including fibrosis, has been shown even in patients without sustained virusological response. During the last years, the advantages of the so-called support therapy using interferon have been demonstrated in patients with an increased rate in progression of fibrosis. Further research of the factors associated with progression of fibrosis will allow optimization of criteria for patient's antiviral therapy.