Abstract
A significant proportion of end stage liver disease is caused by chronic hepatitis C (HCV) infection. Studies have shown that high baseline interferon-gamma-inducible protein-10 (IP-10) concentration correlates with nonresponse to peginterferon/ribavirin therapy and with first and second phase viral kinetics in patients with chronic hepatitis C infection. IP-10 serum concentrations are good surragete parameters for intrahepatic induction of interferon stimulated gene (ISG) activation. Recently higher IP-10 serum concentrations were described as antagonist forms of IP-10 cleaved by DPPIV (Casrouge et al., JCI 2011).
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