Pathogenesis of hepatitis C: HCV consensus 2007

Abstract

The chronic hepatitis C virus (HCV) infects approximately130 million people worldwide [1]. It is estimated thatapproximately 15% of HCV-infected individuals eliminate thevirus spontaneously, that 25% develop a mild form of thedisease, and that 60% develop the chronic progressive form[2]. The elimination or persistence of HCV infection dependson the balance between the effectiveness, specificity andrapidity of the innate and adaptive immune responses, as wellas on the HCV replication rate [3]. Persistence of HCV canalso be caused by infection at privileged (extrahepatic) sites,viral inhibition of antigen presentation, selective immunesuppression, negative regulation of HCV gene expression,viral mutations, immune exhaustion of T cells and theincomplete differentiation of memory T cells [4,5].Fibrosis is the principal complication of chronic hepatitisC, and it is estimated that 20% of patients develop cirrhosisover a period of 10, 20 or 30 years [2,6]. The progression offibrosis increases morbidity and mortality in chronic hepatitisC [7], since it can lead to death due to complications causedby cirrhosis or hepatocarcinoma [2].Various studies have associated the progression of fibrosisin hepatitis C with diverse factors such as: the kinetics andpathogenicity of HCV; host-HCV interaction; intrinsic hostfactors such as demographic profile, body mass index anddiabetes mellitus; host exposure to external factors; and theform of HCV acquisition.