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.

利什曼原虫寄生虫在白蛉载体中复制为有鞭毛的细胞外前鞭毛体，然后在脊椎动物宿主中分化为无鞭毛的细胞内无鞭毛体。前鞭毛体依靠从头合成来产生大部分脂质，包括甘油磷脂、甾醇和鞘脂。相比之下，无鞭毛体从宿主获得大部分脂质，尽管它们保留了一些从头合成的能力。从头合成到抢救的转变反映了利什曼原虫从快速复制的前鞭毛体到生长缓慢、代谢静止的无鞭毛体的转变。未来的研究将揭示无鞭毛体在细胞和分子水平上对宿主脂质的摄取和重塑。阻断脂质从宿主到寄生虫的转移可能提供一种控制利什曼原虫生长的新策略。