Published online Sep 8, 2015. doi: 10.4254/wjh.v7.i19.2202
Peer-review started: June 26, 2015
First decision: August 3, 2015
Revised: August 14, 2015
Accepted: August 30, 2015
Article in press: August 31, 2015
Published online: September 8, 2015
Hepatitis C virus (HCV) infection causes tremendous morbidity and mortality with over 170 million people infected worldwide. HCV gives rise to a sustained, chronic disease in the majority of infected individuals owing to a failure of the host immune system to clear the virus. In general, an adequate immune response is elicited by an efficient antigen presentation by dendritic cells (DCs), the cells that connect innate and adaptive immune system to generate a specific immune response against a pathogen. However, HCV seems to dysregulate the activity of DCs, making them less proficient antigen presenting cells for the optimal stimulation of virus-specific T cells, hence interfering with an optimal anti-viral immune response. There are discordant reports on the functional status of DCs in chronic HCV infection (CHC), from no phenotypic or functional defects to abnormal functions of DCs. Furthermore, the molecular mechanisms behind the impairment of DC function are even so not completely elucidated during CHC. Understanding the mechanisms of immune dysfunction would help in devising strategies for better management of the disease at the immunological level and help to predict the prognosis of the disease in the patients receiving antiviral therapy. In this review, we have discussed the outcomes of the interaction of DCs with HCV and the mechanisms of DC impairment during HCV infection with its adverse effects on the immune response in the infected host.
Core tip: Infection with hepatitis C virus (HCV) is linked with serious outcome like chronic hepatitis in the majority of infected cases, leading to severe liver necrosis and an increased threat of cirrhosis and hepatocellular carcinoma. An aberrant signalling through an inefficient antigen presentation by dendritic cells (DCs) can lead to a subdued T cell immune response. There is a need to completely understand the mechanistic aspects of DC impairment during HCV infection so as to harness this critical arm of the immune system for successful resolution of disease.