Abstract
Leishmania parasites replicate as flagellated, extracellular promastigotes in the sand fly vector and then differentiate into non-flagellated, intracellular amastigotes in the vertebrate host. Promastigotes rely on de novo synthesis to produce the majority of their lipids including glycerophospholipids, sterols and sphingolipids. In contrast, amastigotes acquire most of their lipids from the host although they retain some capacity for de novo synthesis. The switch from de novo synthesis to salvage reflects the transition of Leishmania from fast-replicating promastigotes to slow-growing, metabolically quiescent amastigotes. Future studies will reveal the uptake and remodeling of host lipids by amastigotes at the cellular and molecular levels. Blocking the lipid transfer from host to parasites may present a novel strategy to control Leishmania growth.