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Hepatitis C virus (HCV) infection is one of the most serious public health problems in the world. HCV leads patients to develop hepatic cirrhosis and precipitates hepatocellular carcinoma. HCV establishes persistent infection by impairing host innate and adaptive immune responses. HCV infected hepatocytes sense the infection through Pathogen Associated Molecular Patterns (PAMPs). The sensor molecules, Pattern Recognition Receptors (PRRs) contain two distinct categories, toll like receptors (TLR) and cytoplasmic Retinoic Acid inducible Gene I (RIG-I) like helicases (RLHs). In the hepatocyte, the cytoplasmic PRR, Retinoic Acid inducible Gene I (RIG-I) plays the central role of HCV viral genome recognition, resulting in activation of signaling to induce type I interferon and proinflammatory cytokines. Type I IFN induces more than 300 effector molecules known as interferon stimulated genes (ISGs) that establish an antiviral state in infected cells and neighboring cells. The activation of innate immunity is also critical for the mounting of innate and adaptive immunity. However, a variety of viral strategies of HCV disrupt host innate immune signaling and ISG function, resulting in a dysfunctional immune response against HCV and poor responses to the current type I IFN based therapy. Many studies have reported immune dysfunction during HCV infection in cell culture, animal models and patients. This review article focuses on understanding how the hepatic innate immunity sensor, PRR, associates with HCV PAMPs, and how HCV escapes from host immunity.