Chronic hepatitis C infection is a systemic disease that leads to a high risk of cirrhosis and hepatic carcinoma, as well as extrahepatic related disorders, immune –related and metabolic alterations such as glucose metabolism impairment and steatosis, thus being a new cardio-metabolic risk factor. It has been shown that, due to chronic inflammation, HCV infection has a direct effect on the arterial wall, initiating endothelial dysfunction which is the first step in atherosclerotic processes with proatherogenic effects and numerous cardiovascular events. The recent data emphasize that HCV infection can induce insulin resistance in the liver and peripheral tissues through multiple mechanisms which interfere with insulin signaling, inducing the production of several proinflammatory cytokines, and modify the lipid metabolism with the result of hepatic steatosis, which is more pronounced in patients with HCV. The emergence of new direct acting, interferon-free antiviral treatment, leading to HCV cure in most cases with a satisfactory safety profile is, according to numerous studies, improving the glucose metabolism disorders and lowering the number of cardiovascular events in patients who obtained sustained viral response, thiugh further studies are needed to clarify definitively the role of HCV infection in cardiovascular and metabolic alterations, as well as the impact of viral eradication on cardiovascular outcomes.


hepatitis C virus, cardiometabolic risk, insulin resistance