Mechanisms involved in liver damage resolution after hepatitis C virus clearance

Abstract

Worldwide, the hepatitis C virus (HCV) infection is a leading etiology of cirrhosis and hepatocellular carcinoma (HCC). The main complications of chronic HCV infection are fibrosis, cirrhosis and HCC. Nowadays, there are several options accessible for HCV treatment, such as direct-acting antiviral agents (DAAs), including HCV protease inhibitors, polymerase inhibitors, and NS5A inhibitors. Once the virus is eliminated after the specific antiviral treatments, patients should try to re-establish their metabolic functions efficiently from an environment where there was great cellular destruction. Another goal for the liver can range from fibrosis to decompensate cirrhosis. For this reason, upon the use of DAAs therapy, assuming that SVR is reached, the use of antifibrotic drugs is increasing in order to improve liver regeneration by decreasing fibrotic tissue generated by HCV. Liver fibrosis is defined as the excessive accumulation of extracellular matrix proteins because of the interaction of a number of different cell types, among them hepatic stellate cells. Once the causative agent of damage is removed, the progression of liver disease is attenuated. However, if the patient has an advanced state of fibrosis or cirrhosis, hepatic regeneration becomes a challenge where numerous known and unknown cellular mechanisms are involved. Fortunately, there are drugs that facilitate this process of reversion, however, it is still not clear that conditions favor the success of this regression.