Hepatitis C virus (HCV) is an oncogenic virus that enters the hepatocyte and replicates by altering the cell polarity machinery. While these changes are pretty clearly defined, their effects on the disease's progression are rarely established. Since the introduction of direct acting antivirals in 2012, HCV infection has been effectively treated (DAA). Despite this, patients who have been free of HCV infection are nonetheless at significant risk of developing hepatocellular carcinoma (HCC). Importantly, despite a sustained virologic response (SVR), some of the deregulations induced by HCV are maintained, including the down-regulation of some hepatocyte functions such as bile acid metabolism, exemplifying cell dedifferentiation, and the up-regulation of the epithelial�mesenchymal transition, exemplifying cell dedifferentiation (EMT) EMT is a process in which epithelial cells lose their differentiation and particular polarity in order to acquire mesenchymal cell characteristics such as motility and extracellular matrix remodelling. It's worth noting that epithelial cell polarity functions as a barrier to EMT. As a result, it's crucial to figure out how HCV affects polarity and promotes EMT, which could play a role in viral-induced hepatic carcinogenesis. In this overview, we describe the fundamental phases involved in epithelial cell polarisation and recall the key cellular players involved. We also discuss the characteristics of hepatocyte polarity, which are responsible for their distinct appearance. The effects of HCV on epithelial cell polarity and the repercussions of hepatocyte transformation in the carcinogenesis process are then discussed.
