Department of Microbiology, The University of Chicago, Chicago, IL 60637, USA.
Viruses. 2011 Aug;3(8):1332-41. doi: 10.3390/v3081332. Epub 2011 Aug 4.
Several independent groups have published that autophagy is required for optimal RNA replication of dengue virus (DENV). Initially, it was postulated that autophagosomes might play a structural role in replication complex formation. However, cryo-EM tomography of DENV replication complexes showed that DENV replicates on endoplasmic reticulum (ER) cisternae invaginations and not on classical autophagosomes. Recently, it was reported that autophagy plays an indirect role in DENV replication by modulating cellular lipid metabolism. DENV-induced autophagosomes deplete cellular triglycerides that are stored in lipid droplets, leading to increased β-oxidation and energy production. This is the first example of a virus triggering autophagy to modulate cellular physiology. In this review, we summarize these data and discuss new questions and implications for autophagy during DENV replication.
已有多个独立研究小组发表报告指出，自噬作用是登革热病毒（DENV）实现最佳 RNA 复制所必需的。最初，人们推测自噬体可能在复制复合物形成中发挥结构作用。然而，对 DENV 复制复合物的低温电子显微镜断层扫描显示，DENV 是在内质网（ER）腔陷凹上而非在经典自噬体上进行复制。最近有报道称，自噬作用通过调节细胞脂质代谢间接影响 DENV 的复制。DENV 诱导的自噬体消耗储存在脂滴中的细胞甘油三酯，导致β氧化和产能增加。这是病毒触发自噬作用来调节细胞生理学的首例范例。在本综述中，我们总结了这些数据，并讨论了自噬作用在 DENV 复制过程中的新问题和意义。
