Viruses infect host circumventing the host immune system; a variety of strategies for establishment of viral infection have been found in a virus-specific fashion. Infection with RNA viruses allows host dendritic cells to present antigens and a typical pattern (PAMP) of virus products, including the RNA genomes and replication intermediates such as double-stranded RNA (dsRNA), which induce antiviral effectors: type I interferons (IFN), cytokines, NK cell activation, Th1 polarization, CD8 T cell proliferation, etc. These findings revealed that RNA-sensing innate system closely links to a trigger of cellular immunity. This process unequivocally involves the maturation of antigen-presenting dendritic cell (mDC), and virus products frequently block this step. According to these findings, mDC have to sense non-self RNA to establish antiviral immunity without spoiling their functions via infection, except several exceptional cases. The notion infers that the RNA recognition in cytosol of infected cells (intrinsic sensing) functions as virocidal whereas that in mDC (extrinsic sensing) differentially converges on another antiviral strategy, activation of the immune system. In this review, we focus on the potential role of hepatitis C virus (HCV) RNA in modulating the inflammatory milieu around mDCs and evoking antiviral immunity to drive specific cellular effectors against the virus.