1. ¹Centre for Infection and Inflammation Research, School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia
2. ²Department of Infectious Diseases, Prince of Wales Hospital, Randwick, New South Wales, Australia
3. ³Viral Immunology Group, The Burnet Institute, Melbourne, Victoria, Australia
4. ⁴Virology Division, SEALS, Prince of Wales Hospital, Randwick, New South Wales, Australia
5. ⁵Department of Microbiology & Pathology, Beirne Carter Center for Immunology Research, University of Virginia Health Sciences Center, Charlottesville, VA, USA

Correspondence: Professor A Lloyd, Centre for Infection and Inflammation Research, School of Medical Sciences, University of New South Wales, Sydney, New South Wales 2052, Australia. E-mail: a.lloyd@unsw.edu.au

Received 3 October 2006; Accepted 5 October 2006; Published online 28 November 2006.

Abstract

Individuals infected with hepatitis C virus (HCV) have two possible outcomes of infection, clearance or persistent infection. The focus of this review is the host mechanisms that facilitate clearance. The interaction between HCV viral components and the immune system ultimately determines the balance between the virus and host. Strong evidence points to the aspects of cellular immune response as the key determinants of outcome. The recent discovery of viral evasion strategies targeting innate immunity suggests that the interferon-/ induction pathways are also critical. A growing body of evidence has implicated polymorphisms in both innate and adaptive immune response genes as determinants of viral clearance in individuals infected with HCV.