Sphingolipids. Although originally known as vital components of barrier membranes, sphingolipids are also potent bioactive molecules that regulate cell death, growth, differentiation and intracellular trafficking [32] [33] . The primary sphingolipids regulated during DENV infection were sphingomyelin (SM) and ceramide (CER). In DENV infected cells, SM was up regulated by ,2-fold compared to the controls (UV-DENV and mock) and remained elevated at both 36 hr and 60 hr time points ( Figure 3A and B). Furthermore, this temporal expression varied depending on the specific molecular species being expressed ( Figure 3E and Table S1 ). UV-DENV exposed cells showed similar levels of SM compared to the mock at the 36 hr time point, but these levels decreased at the later time point. Interestingly, an analog of SM known as ceramide phosphoethanolamine (CER-PE), was preferentially expressed (up regulated by ,2 fold) in UV-DENV exposed cells at the 36 hr time point (compared to DENV and mock) ( Figure 3G ). However, this expression level dropped below the mock at the later time point. In comparison, DENV infected cells showed very low expression of this lipid at the early time point (,0.7 fold compared to mock) and its expression was undetectable at the later time point ( Figure 3A and B). This lipid is expressed more abundantly in insect cells rather than in mammalian cells [23] [24] .