Background
Plasmacytoid dendritic cells (pDCs) are responsible for the production of type I IFN during viral infection. Viral elimination by IFN-alpha-based therapy in more than 50% of patients chronically infected with hepatitis C virus (HCV) suggests a possible impairment of production of endogenous IFN-alpha by pDCs in infected individuals. Recent studies in the HCVcc-exposed pDCs purified from healthy donors show that HCV is a weak inducer of IFN-alpha in vitro and that HCVcc blocks the TLR9-mediated IFN-alpha production. It has been also reported that PI3K/AKT is critical for type I IFN production by pDCs in response to TLR agonists. The specific aim of the present study is to investigate the effect of HCV on PI3K/AKT signaling.