We had previously shown that fatty acid biosynthesis was a key target of DENV in human cells and that the rate limiting enzyme, fatty acid synthase (FAS), was both required and re-localized to sites of viral RNA replication during DENV infection [20] . In this study, using an inhibitor of FAS, C75, we determined that this requirement for fatty acid biosynthesis was conserved between the host and its vector during DENV infection. In the presence of C75 DENV replication was significantly reduced in C6/36 mosquito cells indicating that fatty acid biosynthesis is important for virus viability ( Figure 1A ). Furthermore, a time course of addition of C75 ( Figure 1B ) indicated that while pre-treatment or treatment of cells with C75 during viral adsorption reduced virus replication by ,10-100 fold, the most significant effect occurred upon addition of the drug at 4 and 8 hr post-infection (,1000 fold). This suggested that a post-entry step was affected by the inhibition of FAS. A comparison of virus released into the supernatant to intracellular virus indicated that an accumulation of intracellular virus was not occurring in the C75 treated cells (data not shown). Thus, the block in replication was not at the level of virus assembly or release.