Department of Microbiology, The University of Chicago, Chicago, IL 60637, USA.
Cell Host Microbe. 2010 Nov 18;8(5):422-32. doi: 10.1016/j.chom.2010.10.006.
Autophagy influences numerous cellular processes, including innate and adaptive immunity against intracellular pathogens. However, some viruses, including dengue virus (DENV), usurp autophagy to enhance their replication. The mechanism for a positive role of autophagy in DENV infection is unclear. We present data that DENV induction of autophagy regulates cellular lipid metabolism. DENV infection leads to an autophagy-dependent processing of lipid droplets and triglycerides to release free fatty acids. This results in an increase in cellular β-oxidation, which generates ATP. These processes are required for efficient DENV replication. Importantly, exogenous fatty acids can supplant the requirement of autophagy in DENV replication. These results define a role for autophagy in DENV infection and provide a mechanism by which viruses can alter cellular lipid metabolism to promote their replication.
自噬影响众多细胞过程，包括固有和适应性免疫应答以抵抗细胞内病原体。然而，一些病毒，包括登革热病毒（DENV），利用自噬来增强其复制。自噬在 DENV 感染中发挥积极作用的机制尚不清楚。我们提供的数据表明，DENV 诱导的自噬调节细胞脂质代谢。DENV 感染导致脂滴和甘油三酯的自噬依赖性加工，以释放游离脂肪酸。这导致细胞β-氧化增加，从而产生 ATP。这些过程对于 DENV 的有效复制是必需的。重要的是，外源性脂肪酸可以替代自噬在 DENV 复制中的需求。这些结果定义了自噬在 DENV 感染中的作用，并提供了一种机制，病毒可以通过改变细胞脂质代谢来促进其复制。
