Dengue virus is one of the most aggressive human pathogens worldwide. It causes 50-100 million infections per year but there is no vaccine or antiviral that is currently effective against the disease. The virus is spread by Aedes aegyptii and Aedes albopictus mosquitoes and viral replication within the mosquito vector is required for transmission to a new human host. During this replication cycle, the virus causes significant changes to the membrane organization of infected cells. These virus-induced membrane alterations help to assemble arrays of viral replication factories and aid the virus to evade host antiviral defense mechanisms. Previously, much effort has been placed in trying to identify viral and cellular protein effectors that aid virus replication. In this study we have explored the role of lipids in the formation of these extensive membrane platforms in mosquito cells. Using high-resolution mass spectrometry we have profiled the lipid composition of dengue virus infected mosquito cells and compared it to uninfected cells. Through this we have identified several lipid classes that are differentially regulated during dengue virus replication. Using inhibitors of lipid biosynthesis we have also identified a lipid repertoire that is inhibitory to viral replication. Knowledge of how dengue virus utilizes cellular lipids and downstream signaling pathways to facilitate its replication will provide novel targets that could be utilized for developing effective antivirals. This study is also a forerunner for future comparative analyses of the human host and vector membrane environments required for viral replication. 15% of the metabolites identified were significantly (Anova p,0.05) different between virus infected cells and the mock control.