Hepatitis C virus infection upregulates expression of the type I interferon receptor in human peripheral blood mononuclear cells

Abstract

To assess whether hepatitis C virus infection (HCV) affects type I interferon (IFN) receptor expression, the expression levels of two subunits of this receptor, IFNAR1 and IFNAR2, in peripheral blood mononuclear cells (PBMCs) were determined by flow-cytometric assay in 68 anti-HCV antibody-positive patients (47 positive for HCV RNA and 21 negative for HCV RNA) and 14 healthy controls. The percentages of IFNAR1- and IFNAR2-expressing cells were significantly higher in HCV RNA-positive patients than in HCV RNA-negative patients or healthy controls. In multiple regression analysis, the presence of HCV RNA in serum was independently associated with the expression of both IFNAR1 and IFNAR2 in PBMCs ( P=0.007 for IFNAR1 and P=0.003 for IFNAR2). The frequency of IFN-γ-producing peripheral CD4 + and CD8 + cells was also significantly higher in HCV RNA-positive patients than in HCV RNA-negative patients or healthy controls and there was a significant correlation between IFN receptor expression and the frequency of IFN-γ-producing cells. These results suggest that HCV infection upregulates the expression of the type I IFN receptor in PBMCs through enhanced IFN-γ production by peripheral CD4 + and CD8 + cells as one of mechanisms that regulate the expression of the type I IFN receptor.