Hepatitis C Virus and Human Herpesvirus 8: Immunological Response, Modification of Cell Metabolism and Association with Type 2 Diabetes

Oncogenic and latent-persistent viruses belonging to both DNA (herpesviruses) and RNA viruses [hepatitis C virus (HCV), enteroviruses, rubella, human immunodeficiency virus, and dengue virus] are known to cause severe alterations of cell metabolism, which occasionally can lead to diabetes onset. HCV has been claimed to be able to impair cell metabolism by means of a direct modification of insulin cell sensitivity and host innate immune response. Human herpesvirus 8 (HHV8) infection also induces stable modifications in cell metabolism. HHV8 enhances the production of insulin receptors in endothelial cells, favors the concentration of lipid droplets in the cytoplasm of endothelial cells, and induces a general impairment of both triglycerides and cholesterol metabolism. HHV8 is also known to alter humoral response and the production of cytokines, which affects cell oxidative activity (reactive oxygen species activation), with a general impairment of acquired immunity. This review focuses particular attention on the recent findings reported on these two latent-persistent human viruses, namely, HCV and HHV8.