Replication of the hepatitis C virus (HCV) strongly relies on various lipid metabolic processes in different steps of the viral life cycle. In general, HCV changes the cells’ lipidomic profile by differentially regulating key pathways of lipid synthesis, remodeling, and utilization. In this review, we sum up the latest data mainly from the past five years, emphasizing the role of lipids in HCV RNA replication, assembly, and egress. In detail, we highlight changes in the fatty acid content as well as alterations of the membrane lipid composition during replication vesicle formation. We address the role of lipid droplets as a lipid provider during replication and as an essential hub for HCV assembly. Finally, we depict different ideas of HCV maturation and egress including lipoprotein association and potential secretory routes.

Protein tyrosine phosphatase 1B (PTP1B) is a negative regulator of the leptin and insulin signalling pathways. This phosphate is of great interest as PTP1B knockout mice are protected against the development of obesity and diabetes. Here, we provide evidence for a novel function of PTP1B, which is independent of its phosphatase activity, but requires its localisation to the membrane of the endoplasmic reticulum. Upon activation of pattern recognition receptors, macrophages and plasmacytoid dendritic cells from PTP1B knockout mice secrete lower amounts of type I interferon (IFN) than cells from wild type mice. In contrast, secretion of proinflammatory cytokines TNFα and IL-6 was unaltered. While PTP1B deficiency did not affect IFNb1 transcription, type I IFN accumulated in macrophages, suggesting a role for PTP1B in mediating secretion of type I IFN. In summary, we have uncovered that PTP1B positively regulates the type I IFN response by promoting secretion of key antiviral cytokines.