Recent studies support the notion that glycolysis and oxidative phosphorylation are rheostats in immune cells whose bioenergetics have functional outputs in terms of their biology. Specific intrinsic and extrinsic molecular factors function as molecular potentiometers to adjust and control glycolytic to respiratory power output. In many cases, these potentiometers are used by influenza viruses and immune cells to support pathogenesis and the host immune response, respectively. Influenza virus infects the respiratory tract, providing a specific environmental niche, while immune cells encounter variable nutrient concentrations as they migrate in response to infection. Immune cell subsets have distinct metabolic programs that adjust to meet energetic and biosynthetic requirements to support effector functions, differentiation, and longevity in their ever-changing microenvironments. This review details how influenza coopts the host cell for metabolic reprogramming and describes the overlap of these regulatory controls in immune cells whose function and fate are dictated by metabolism. These details are contextualized with emerging evidence of the consequences of influenza-induced changes in metabolic homeostasis on disease progression.

中文翻译：

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加剧流感和免疫反应：流感感染和免疫代谢过程中代谢重编程的含义。

最近的研究支持以下观点：糖酵解和氧化磷酸化是免疫细胞中的变阻器，其生物能学在生物学方面具有功能性输出。特定的内在和外在分子因素起分子电位计的作用，以调节和控制糖酵解对呼吸动力的输出。在许多情况下，流感病毒和免疫细胞使用这些电位计分别支持发病机制和宿主免疫反应。流感病毒感染呼吸道，提供特定的环境环境，而免疫细胞在响应感染而迁移时会遇到不同的营养物浓度。免疫细胞亚群具有独特的代谢程序，这些程序可以进行调整以满足能量和生物合成的要求，以支持效应子功能，分化，在不断变化的微环境中长寿。这篇综述详细描述了流感病毒如何通过宿主细胞进行代谢重编程，并描述了这些调节控制在免疫细胞中的重叠，这些免疫细胞的功能和命运取决于新陈代谢。这些细节与流行性感冒引起的代谢稳态变化对疾病进展的后果的新兴证据相关联。