Although the immune system can clear hepatitis C virus, infection oftencarries forward into a chronic phase. Chronic HCV is inducing dysregulation of adaptive and innate immune response, antiviral cytotoxicity and hepatocyte apoptosis in the liver, whichtogether reflects to a infection outcome and therapy efficassy and probablycontribute to hepatic fibrosis and cirrhosis. HCV achives thisimmune system dysregulation by escaping the host immune response at different points to inhibit the initial coordination of immunitythat induces the whole immune response, including adaptive, specific immunity,which anablesthe increase of the viral replication and contributes to establishment of chronic infection. Within the liver tissue environment, multiple immune cell typescontribute to the antiviral response toward HCV. A prevention of any part of the innate immune response by HCV could resultby an ineffective immunity, both in natural HCV clearance and virus clearance during the treatment, what could anable the infection to progress toa liverdisease. A full understanding of how viral modulationof immune system affects HCV infection outcome will require identification of the numerous antiviraland immunomodulatory cytokines that mediate the cross-talk betweenthe various immune and non-immune cell types within the complex hepatic tissue. Research to continue in these discoveries and developments are focused to reveal the key factors required for successful antiviral immunity to HCV. In the ongoing age of personalized medicine, this knowledge could lead to individually made HCV therapies based on knowledge of both viral strategiesand host characteristics. A detailed understanding of these components of an effective immunity to HCV at the non-specific and adaptive levels will be useful tool to guide the research development of the long-desired HCV vaccine.