Atherosclerosis as Extrahepatic Manifestation of Chronic Infection with Hepatitis C Virus

Figure 1

Possible mechanisms connecting HCV infection and cardiovascular disease. HCV is considered a “metabolic” virus and is associated with metabolic disorders, in particular insulin resistance and type 2 diabetes mellitus, which are proatherogenic conditions. By inducing hepatic injury and activating peripheral blood mononuclear cells (PBMC), HCV increases circulating levels of proinflammatory cytokines, leading to peripheral IR and hyperinsulinemia. Furthermore, a key feature of HCV infection is associated with hyperhomocysteinaemia, hypoadiponectinaemia, oxidative stress, lipid peroxidation, and all components of the metabolic syndrome. Therefore, “viral” induced and “metabolic” steatosis, together with the direct stimulus of increased insulin levels on hepatic stellate cells (HSCs) likely stimulate the progression of fibrosis within the liver parenchyma. Furthermore, systemic inflammation, the procoagulative state, and direct viral effects on the vascular wall may contribute to the development and progression of the atherogenic process.