SARS‐CoV‐2 is a novel betacoronavirus that has caused the global health crisis known as COVID‐19. The implications of mitochondrial dysfunction with COVID‐19 are discussed as well as deregulated mitochondria and inter‐organelle functions as a posited comorbidity enhancing detrimental outcomes. Many environmental chemicals (ECs) and endocrine‐disrupting chemicals can do damage to mitochondria and cause mitochondrial dysfunction. During infection, SARS‐CoV‐2 via its binding target ACE2 and TMPRSS2 can disrupt mitochondrial function. Viral genomic RNA and structural proteins may also affect the normal function of the mitochondria‐endoplasmic reticulum‐Golgi apparatus. Drugs considered for treatment of COVID‐19 should consider effects on organelles including mitochondria functions. Mitochondrial self‐balance and clearance via mitophagy are important in SARS‐CoV‐2 infection, which indicate monitoring and protection of mitochondria against SARS‐CoV‐2 are important. Mitochondrial metabolomic analysis may provide new indicators of COVID‐19 prognosis. A better understanding of the role of mitochondria during SARS‐CoV‐2 infection may help to improve intervention therapies and better protect mitochondrial disease patients from pathogens as well as people living with poor nutrition and elevated levels of socioeconomic stress and ECs.

中文翻译：

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健康差异人群对 COVID-19 的易感性：可能与线粒体疾病、社会经济压力和污染物有关。

SARS-CoV-2 是一种新型 β 冠状病毒，引起了被称为 COVID-19 的全球健康危机。讨论了 COVID-19 导致的线粒体功能障碍的影响，以及线粒体和细胞器间功能失调（作为假定的合并症，会增强有害结果）。许多环境化学物质 (EC) 和内分泌干扰化学物质会对线粒体造成损害并导致线粒体功能障碍。在感染过程中，SARS-CoV-2 通过其结合靶点 ACE2 和 TMPRSS2 可以破坏线粒体功能。病毒基因组RNA和结构蛋白也可能影响线粒体-内质网-高尔基体的正常功能。考虑用于治疗 COVID-19 的药物应考虑对细胞器（包括线粒体功能）的影响。线粒体自我平衡和通过线粒体自噬的清除在 SARS-CoV-2 感染中很重要，这表明监测和保护线粒体免受 SARS-CoV-2 的影响很重要。线粒体代谢组学分析可能提供 COVID-19 预后的新指标。更好地了解线粒体在 SARS-CoV-2 感染过程中的作用可能有助于改善干预疗法，更好地保护线粒体疾病患者以及营养不良、社会经济压力和 EC 水平升高的人们免受病原体侵害。