Immune Responses and Immunopathology of Acute and Chronic Hepatitis C Virus Infection

An ample understanding of the HCV life cycle and infection biology has also significantly increased our knowledge of hepatitis C immune responses against acute infection to the progression of chronic hepatitis C and associated comorbidities. As expected in chimpanzees (the best in vivo model so far to study hepatitis C infection kinetics, molecular pathogenesis, and immunopathology) and humans, several arms of the immune responses are activated following HCV infection. Some of the underlying mechanisms both for innate immune responses and adaptive immune responses to viral clearance and persistent HCV infection are fully understood, however; some fundamental questions in hepatitis C immunopathology remain to be answered and some immune responses hypothesis demands further studies to validate. Some mechanistic issues of viral evasion strategies during infection progression and the future development of prophylactic and protective anti-HCV vaccines will be largely dependent on the full understanding of the kinetics of adaptive immune responses against HCV infection. As generally presumed the inefficient role of innate immunity in self-resolving HCV infection, the potent immune responses of CD8+ T and CD4+ T cells are critically important after the acute phase of the infection. In particular, the plausible understanding of CD4+ T cells responses against persistent infection will certainly be central to the development of future HCV vaccines. In this chapter, we overview the host immune responses against hepatitis C acute infection and subsequent CHC infection, their regulation by viral and cellular proteins, and the virus purging strategies while impairing host defense system mechanisms.

Keywords: Adaptive immune response, Anergy, Anti-HCV vaccines, Crossreactive neutralizing antibodies, CD+ 4 T cells, CD+ 8 T cells, Dendritic cells, Cytotoxic T lymphocyte, Hepatitis C virus, Host-immune response, Immunoregulatory cells, Immunopathogenesis, Innate immune response, Natural killer cells, Priming, Protective vaccines, Prophylactic vaccines, T-cell exhaustion, Viral escape.