Centro de Investigación Veterinaria de Tandil (CIVETAN), UNCPBA-CICPBA-CONICET, Campus Universitario, Tandil CC7000, Buenos Aires, Argentina.
Department of Drug Discovery & Biomedical Sciences, Medical University of South Carolina, DD 506 Drug Discovery Building, 70 President Street, MSC 139, Charleston, SC 29425, USA.
Cells. 2024 Oct 29;13(21):1789. doi: 10.3390/cells13211789.
Viruses are intracellular parasites that utilize organelles, signaling pathways, and the bioenergetics machinery of the cell to replicate the genome and synthesize proteins to build up new viral particles. Mitochondria are key to supporting the virus life cycle by sustaining energy production, metabolism, and synthesis of macromolecules. Mitochondria also contribute to the antiviral innate immune response. Here, we describe the different mechanisms involved in virus-mitochondria interactions. We analyze the effects of viral infections on the metabolism of glucose in the Warburg phenotype, glutamine, and fatty acids. We also describe how viruses directly regulate mitochondrial function through modulation of the activity of the electron transport chain, the generation of reactive oxygen species, the balance between fission and fusion, and the regulation of voltage-dependent anion channels. In addition, we discuss the evasion strategies used to avoid mitochondrial-associated mechanisms that inhibit viral replication. Overall, this review aims to provide a comprehensive view of how viruses modulate mitochondrial function to maintain their replicative capabilities.
病毒是细胞内寄生虫，利用细胞器、信号通路和细胞的生物能量机制来复制基因组并合成蛋白质以构建新的病毒颗粒。线粒体通过维持能量产生、代谢和大分子合成来支持病毒生命周期，是关键。线粒体也有助于抗病毒的先天免疫反应。在这里，我们描述了病毒-线粒体相互作用中涉及的不同机制。我们分析了病毒感染对葡萄糖代谢、谷氨酰胺和脂肪酸的瓦伯格表型的影响。我们还描述了病毒如何通过调节电子传递链的活性、活性氧的产生、分裂和融合的平衡以及电压依赖性阴离子通道的调节来直接调节线粒体功能。此外，我们还讨论了用于逃避抑制病毒复制的线粒体相关机制的逃避策略。总的来说，本综述旨在提供一个全面的视角，了解病毒如何调节线粒体功能以维持其复制能力。
