Open AccessAdaptive immune response during hepatitis C virus infection
Author(s) -
J.R. Larrubia,
Elia Moreno-Cubero,
M.U. Lokhande,
Silvia García-Garzón,
Alicia Lázaro,
J. Míquel,
Cristian Perna,
E. Sanz-de-Villalobos
Publication year - 2014
Publication title -
world journal of gastroenterology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v20.i13.3418
Subject(s) - immune system , immunology , hepatitis c virus , virology , biology , acquired immune system , virus , cytotoxic t cell , epitope , antibody , t cell , biochemistry , in vitro
Hepatitis C virus (HCV) infection affects about 170 million people worldwide and it is a major cause of liver cirrhosis and hepatocellular carcinoma. HCV is a hepatotropic non-cytopathic virus able to persist in a great percentage of infected hosts due to its ability to escape from the immune control. Liver damage and disease progression during HCV infection are driven by both viral and host factors. Specifically, adaptive immune response carries out an essential task in controlling non-cytopathic viruses because of its ability to recognize infected cells and to destroy them by cytopathic mechanisms and to eliminate the virus by non-cytolytic machinery. HCV is able to impair this response by several means such as developing escape mutations in neutralizing antibodies and in T cell receptor viral epitope recognition sites and inducing HCV-specific cytotoxic T cell anergy and deletion. To impair HCV-specific T cell reactivity, HCV affects effector T cell regulation by modulating T helper and Treg response and by impairing the balance between positive and negative co-stimulatory molecules and between pro- and anti-apoptotic proteins. In this review, the role of adaptive immune response in controlling HCV infection and the HCV mechanisms to evade this response are reviewed.