Liu Xueao, Chen Li, Niu Honglin, Chen Yuhan, Chen Peiyao, Liu Lei, Wu Rui
Jiamusi University of Basic Medicine, Jiamusi University, Jiamusi, Heilongjiang, China.
The Affiliated First Hospital, Jiamusi University, Jiamusi, Heilongjiang, China.
Virulence. 2025 Dec;16(1):2554302. doi: 10.1080/21505594.2025.2554302. Epub 2025 Sep 3.
Viral particles and proteins released during infection profoundly reshape the cellular microenvironment by disrupting host signaling, triggering inflammation, and modulating immune responses. Glucose metabolism, a critical hub for energy production and biosynthesis, is highly susceptible to viral reprogramming. This review summarizes recent findings showing that diverse viruses, including influenza virus, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and enteroviruses, manipulate glucose metabolic pathways to promote replication and evade immune surveillance. Specifically, viruses modulate glycolytic flux, alter the activity of key metabolic enzymes such as hexokinase (HK) and pyruvate kinase, and interfere with signaling networks like PI3K/Akt/mTOR and AMPK. These metabolic alterations further impact the immune landscape by regulating cytokine production, immune cell activation, and antiviral responses. Our analysis highlights a bidirectional interaction: while viruses hijack host glucose metabolism to favor their survival, metabolic changes also generate host-derived antiviral responses. This review highlights the bidirectional crosstalk between metabolic remodeling and microenvironmental changes during viral infection, underscoring the potential of metabolism-based antiviral strategies. A deeper understanding of these mechanisms may inform the development of more effective and targeted interventions against viral diseases.
感染期间释放的病毒颗粒和蛋白质通过破坏宿主信号传导、引发炎症和调节免疫反应,深刻地重塑细胞微环境。葡萄糖代谢作为能量产生和生物合成的关键枢纽,极易受到病毒重编程的影响。本综述总结了近期的研究发现,表明包括流感病毒、严重急性呼吸综合征冠状病毒2(SARS-CoV-2)和肠道病毒在内的多种病毒,操纵葡萄糖代谢途径以促进病毒复制并逃避免疫监视。具体而言,病毒调节糖酵解通量,改变关键代谢酶如己糖激酶(HK)和丙酮酸激酶的活性,并干扰PI3K/Akt/mTOR和AMPK等信号网络。这些代谢改变通过调节细胞因子产生、免疫细胞活化和抗病毒反应,进一步影响免疫格局。我们的分析突出了一种双向相互作用:病毒劫持宿主葡萄糖代谢以利于其生存,而代谢变化也会产生宿主源性抗病毒反应。本综述强调了病毒感染期间代谢重塑与微环境变化之间的双向串扰,凸显了基于代谢的抗病毒策略的潜力。对这些机制的更深入理解可能为开发更有效、更具针对性的病毒性疾病干预措施提供依据。