Viruses rely on host lipid metabolic pathways for multiplication. Lipid droplets are the cellular storage organelles of neutral lipids and central hubs of lipid metabolism. Viruses exploit host lipid droplets as source for membrane lipids that form replication organelles or the envelope of virions or for energy to fulfil their replicative cycle. These findings are summarized in this Graphical Review.

Intracellular pathogens rely on host metabolic networks for multiplication. Enveloped viruses need lipids for formation of the viral envelope and positive sense RNA viruses that replicate in membranous inclusions require lipids for formation of the replication compartments. In addition, all intracellular pathogens need energy for their replicative cycle. As triglycerides in lipid droplets are the main energy storage unit of cells and major source of membrane lipids, it is not surprising that viruses have evolved various strategies to exploit different aspects of lipid droplet biology.

Non-alcoholic fatty liver disease (NAFLD) begins with lipid accumulation and progresses toward inflammation and fibrosis. Nuclear receptors (NRs), like the Peroxisome Proliferator-Activated Receptors alpha and gamma (PPARα and PPARy), the Farnesoid X Receptor (FXR), and the Liver X receptor (LXR), regulate genes by heterodimerizing with Retinoid X receptor (RXR). These receptors are emerging targets for pharmaceutical intervention for metabolic diseases.

Proteins which associate with the surface of lipid droplets are intimately involved in the regulation of the droplets. Several human inherited disorders have now been linked to loss- and, in some cases, likely gain-of-function mutations in the genes encoding these proteins. These are summarised in this Graphical Review.

Autophagy degrades or recycles cellular components through the formation of a double membrane vesicle, termed autophagosome, which fuses with the lysosome, where the degradation process takes place. In this Graphical Review we provide an updated and comprehensive overview on autophagosome biogenesis, a unique process consisting of three main phases: nucleation, expansion, and maturation, tightly regulated by lipid species and protein complexes.

Autophagy is an intracellular catabolic process that eliminates cytoplasmic constituents selectively by tight engulfment in an isolation membrane or recycles bulk cytoplasm by nonselective sequestration. Completion of the isolation membrane forms a double membrane vesicle, termed autophagosome, that proceeds to fusion with the lysosome, where the inner membrane and its cytoplasmic content are degraded. Autophagosome biogenesis is unique in that the newly-formed membrane, termed phagophore, is elongated by direct lipid flow from a proximal ER-associated donor membrane. Recent years mark a tremendous advancement in delineating the direct regulation of this process by different lipid species and associated protein complexes. Here we schematically summarize the current view of autophagy and autophagosome biogenesis.