In patients suffering from persistent Hepatitis C Virus (HCV) infection, chronic inflammation resulting from immune responses against infected hepatocytes is associated with progressive fibrosis, cirrhosis and cellular hepatocarcinoma. Several lines of evidence have indicated that direct virus/host interactions are also involved. Thus a combination of virus-specific, host genetic, environmental and immune-related factors are likely to determine progression to HCC in patients who are chronically infected with HCV. Extensive studies have suggested an important role for HCV core protein in HCV-induced liver pathologies. HCV core protein has been reported to interact with several cellular proteins, giving rise to a modulation of different signalling cascades and consequently the modulation of a number of cellular regulatory functions.
In order to understand the mechanisms involved in HCV-induced liver pathologies, and the crosstalk of virus/host interactions, the aim of this research programme is to study:
- The role of HCV core protein in TGF-b mediated biological responses (M.F. Bourgeade)
- The role of phosphoinositides and septins in HCV replication (A. Gassama)
- The role of HCV in immune responses and particularly in HCV/HIV co-infected patients who developed severe fibrosis following transplantation. (Professor A.M. Roque).