Based on available metabolomic studies, influenza infection affects a variety of cellular metabolic pathways to ensure an optimal environment for its replication and production of viral particles. Following infection, glucose uptake and aerobic glycolysis increase in infected cells continually, which results in higher glucose consumption. The pentose phosphate shunt, as another glucose-consuming pathway, is enhanced by influenza infection to help produce more nucleotides, especially ATP. Regarding lipid species, following infection, levels of triglycerides, phospholipids, and several lipid derivatives undergo perturbations, some of which are associated with inflammatory responses. Also, mitochondrial fatty acid β-oxidation decreases significantly simultaneously with an increase in biosynthesis of fatty acids and membrane lipids. Moreover, essential amino acids are demonstrated to decline in infected tissues due to the production of large amounts of viral and cellular proteins. Immune responses against influenza infection, on the other hand, could significantly affect metabolic pathways. Mainly, interferon (IFN) production following viral infection affects cell function via alteration in amino acid synthesis, membrane composition, and lipid metabolism. Understanding metabolic alterations required for influenza virus replication has revealed novel therapeutic methods based on targeted inhibition of these cellular metabolic pathways.

中文翻译：

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流感感染的代谢宿主反应和治疗方法


根据现有的代谢组学研究，流感感染会影响多种细胞代谢途径，以确保其复制和病毒颗粒产生的最佳环境。感染后，受感染细胞的葡萄糖摄取和有氧糖酵解持续增加，导致葡萄糖消耗增加。戊糖磷酸分流是另一种葡萄糖消耗途径，流感感染会增强戊糖磷酸分流，以帮助产生更多的核苷酸，尤其是 ATP。关于脂质种类，感染后，甘油三酯、磷脂和几种脂质衍生物的水平会受到干扰，其中一些与炎症反应有关。此外，线粒体脂肪酸β-氧化显着降低，同时脂肪酸和膜脂生物合成增加。此外，由于大量病毒和细胞蛋白的产生，受感染组织中的必需氨基酸被证明会减少。另一方面，针对流感感染的免疫反应可能会显着影响代谢途径。病毒感染后产生的干扰素 (IFN) 主要通过改变氨基酸合成、膜组成和脂质代谢来影响细胞功能。了解流感病毒复制所需的代谢改变揭示了基于这些细胞代谢途径的靶向抑制的新治疗方法。