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 a
re directed at multiple determinants (polyclonal) involving most of th
e viral antigens. These responses apparently involve neutralizing anti
bodies as well as peripheral and liver infiltrating cytotoxic T lympho
cytes (CD8+) and proliferative reaction associated with CD4+. In most
cases these responses cannot control infection. In addition, re-infect
ion following an episode of self-limited infection or during chronic c
arrier condition has been described in chimpanzees and in man. Among t
he factors that may influence immune response by the host are the poss
ible existence of extra-hepatic sites capable of supporting viral repl
ication (in particular of haematopoietic origin) as well as the existe
nce of complexed viral particles (such as with immunoglobulins and lip
id components).