Pombo Joao Palma, Sanyal Sumana
HKU-Pasteur Research Pole, School of Public Health, The University of Hong Kong, Hong Kong, Hong Kong.
School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.
Front Immunol. 2018 Jun 4;9:1276. doi: 10.3389/fimmu.2018.01276. eCollection 2018.
Cellular lipid homeostasis is maintained through an intricately linked array of anabolic and catabolic pathways. Upon flavivirus infections, these are significantly altered: on the one hand, these viruses can co-opt lipid metabolic pathways to generate ATP to facilitate replication, or to synthesize membrane components to generate replication sites; on the other hand, more recent evidence suggests counter strategies employed by host cells, which actively modulate several of these networks in response to infection, enhancing interferon signaling by doing so, and thus creating an antiviral environment. In this review, we discuss recent data on mechanisms of alteration of lipid metabolic pathways during infection by flaviviruses, with a focus on cholesterol and fatty acid biosynthesis, which can be manipulated by the invading viruses to support replication, but can also be modulated by the host immune system itself, as a means to fight infection.
细胞脂质稳态通过一系列复杂相连的合成代谢和分解代谢途径得以维持。在黄病毒感染时，这些途径会发生显著改变：一方面，这些病毒可利用脂质代谢途径生成ATP以促进复制，或合成膜成分以产生复制位点；另一方面，最新证据表明宿主细胞会采取应对策略，即针对感染主动调节其中一些网络，借此增强干扰素信号传导，从而营造抗病毒环境。在本综述中，我们讨论了有关黄病毒感染期间脂质代谢途径改变机制的最新数据，重点关注胆固醇和脂肪酸生物合成，入侵病毒可操纵这些过程以支持复制，但宿主免疫系统本身也可对其进行调节，以此作为对抗感染的一种手段。
