Published online Dec 21, 2018. doi: 10.3748/wjg.v24.i47.5297
Peer-review started: October 19, 2018
First decision: November 22, 2018
Revised: November 27, 2018
Accepted: November 30, 2018
Article in press: November 30, 2018
Published online: December 21, 2018
Processing time: 63 Days and 7.8 Hours
Hepatitis C virus (HCV) infection commonly causes progressive liver diseases that deteriorate from chronic inflammation to fibrosis, cirrhosis and even to hepatocellular carcinoma. A long-term, persistent and uncontrolled inflammatory response is a hallmark of these diseases and further leads to hepatic injury and more severe disease progression. The levels of inflammatory cytokines and chemokines change with the states of infection and treatment, and therefore, they may serve as candidate biomarkers for disease progression and therapeutic effects. The mechanisms of HCV-induced inflammation involve classic pathogen pattern recognition, inflammasome activation, intrahepatic inflammatory cascade response, and oxidative and endoplasmic reticulum stress. Direct-acting antivirals (DAAs) are the first-choice therapy for effectively eliminating HCV, but DAAs alone are not sufficient to block the uncontrolled inflammation and severe liver injury in HCV-infected individuals. Some patients who achieve a sustained virologic response after DAA therapy are still at a long-term risk for progression to liver cirrhosis and hepatocellular carcinoma. Therefore, coupling with anti-inflammatory/hepatoprotective agents with anti-HCV effects is a promising therapeutic regimen for these patients during or after treatment with DAAs. In this review, we discuss the relationship between inflammatory mediators and HCV infection, summarize the mechanisms of HCV-induced inflammation, and describe the potential roles of anti-inflammatory/hepatoprotective drugs with anti-HCV activity in the treatment of advanced HCV infection.
Core tip: Inflammatory responses triggered by hepatitis C virus (HCV) infection lead to severe progressive liver diseases. Some inflammatory cytokines and chemokines may serve as biomarkers for the disease progression and therapeutic effect in chronic hepatitis C (CHC) patients. The inflammatory pathogenesis in HCV-infected patients is complicated, including classic pathogen pattern recognition, inflammasome activation, intrahepatic inflammatory cascade response, and oxidative and endoplasmic reticulum stress. Direct-acting antivirals (DAAs) are not sufficient to block the uncontrolled inflammation and disease progression in severe CHC patients. Therefore, coupling with anti-inflammatory/hepatoprotective agents with anti-HCV effects is a promising therapeutic regimen for advanced HCV-infected patients during or after treatment with DAAs.