The most pronounced changes are those observed in the 16K pellet analyses where a significant decrease in phospholipids, sphingolipids and lipid intermediates are observed (compared to mock cells, Figure 5A) . A comparison of SM and CER in the whole cell analysis at the 36 hr and 60 hr time points ( Figure 1A and 1B) indicated a reduction in SM with a corresponding increase in CER with time. This could be due to a similar scenario to SINV where a non-replicating UV-DENV is capable of inducing lipid conversion in membranes [52] . Therefore, SM and other sphingolipids may be converted to CER that is transported away from the 16K membrane fraction to other locations in the cell. This is also evident from the increased content of fatty acids compared to mock cells that may result from the degradation of lipids. UV-DENV exposed cells do not show significant regulation of MG or DG, but show an up regulation of palmitic acid (C16:0). Virus binding and entry alone could stimulate lipid droplet hydrolysis (catabolism of TG) resulting in the release of palmitic acid. These studies have shown that UV-DENV could be a versatile tool to pursue mechanistic studies on the metabolic pertabations that occur upon virus binding, membrane fusion, and entry.