Abstract
The immune response triggered by hepatitis C virus (HCV) infection is still poorly documented and its underlying mechanisms are still to be elucidated. Following infection, both humoral and cellular responses are directed at multiple determinants (polyclonal) involving most of the viral antigens. These responses apparently involve neutralizing antibodies as well as peripheral and liver infiltrating cytotoxic T lymphocytes (CD8+) and proliferative reaction associated with CD4+. In most cases these responses cannot control infection. In addition, re-infection following an episode of self-limited infection or during chronic carrier condition has been described in chimpanzees and in man. Among the factors that may influence immune response by the host are the possible existence of extra-hepatic sites capable of supporting viral replication (in particular of haematopoietic origin) as well as the existence of complexed viral particles (such as with immunoglobulins and lipid components).

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