Background: Evidence suggests that Epstein-Barr virus (EBV) plays a role in triggering or perpet-

Hepatitis C virus (HCV) patients have extrahepatic manifestations, such as cryoglobulins. Cryoglubilins are immunoglubulins that precipitate in the cold and contain IgM rheumatoid factor. Vasculitis is an autoimmune manifestation detected in a subset of HCV patients with cryoglobulins (1-5%). HCV patients with mixed cryoglobulinemia have enhanced levels of CXCL10 (a chemotactic ligand of CXCR3) in their plasma (Antonelli.2008) and CXCR3+ B cells are detected in the liver compartment (Mizouchi. 2010). We analyzed by flow cytometric analysis a defined cohort of HCV patients (Cryoglobulin and Rheumatoid factor state) and healthy controls for CXCR3 and CXCR4 expression on B cell subsets. The chemokine expression was compared with parameters of B cell phenotype such as activation state (CD86), and cell cycling(ki-67) . We found that mature activated B cells of HCV patients had a high expression of CXCR3 (75% in HCV vs. 20% in healthy controls).. The goal of this project is to define the potential role that CXCR3 plays in the progression of HCV towards autoimmunity by comparison with alteration in B cell parameters such as alterations of cycling, apoptosis and survival.