Ganji Riya, Reddy P Hemachandra
Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
Departments of Neuroscience and Pharmacology, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
Front Aging Neurosci. 2021 Jan 12;12:614650. doi: 10.3389/fnagi.2020.614650. eCollection 2020.
The coronavirus disease 2019 (COVID-19) has become a deadly pandemic with surging mortality rates and no cure. COVID-19 is caused by the severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) with a range of clinical symptoms, including cough, fever, chills, headache, shortness of breath, difficulty breathing, muscle pain, and a loss of smell or taste. Aged individuals with compromised immunity are highly susceptible to COVID-19 and the likelihood of mortality increases with age and the presence of comorbidities such as hypertension, diabetes mellitus, cardiovascular disease, or chronic obstructive pulmonary disease. Emerging evidence suggests that COVID-19 highjacks mitochondria of immune cells, replicates within mitochondrial structures, and impairs mitochondrial dynamics leading to cell death. Mitochondria are the powerhouses of the cell and are largely involved in maintaining cell immunity, homeostasis, and cell survival/death. Increasing evidence suggests that mitochondria from COVID-19 infected cells are highly vulnerable, and vulnerability increases with age. The purpose of our article is to summarize the role of various age-related comorbidities such as diabetes, obesity, and neurological diseases in increasing mortality rates amongst the elderly with COVID-19. Our article also highlights the interaction between coronavirus and mitochondrial dynamics in immune cells. We also highlight the current treatments, lifestyles, and safety measures that can help protect against COVID-19. Further research is urgently needed to understand the molecular mechanisms between the mitochondrial virus and disease progression in COVID-19 patients.
2019冠状病毒病（COVID-19）已成为一场致命的大流行病，死亡率不断飙升且无治愈方法。COVID-19由严重急性呼吸综合征冠状病毒2（SARS-CoV-2）引起，具有一系列临床症状，包括咳嗽、发热、寒战、头痛、呼吸急促、呼吸困难、肌肉疼痛以及嗅觉或味觉丧失。免疫力受损的老年人极易感染COVID-19，死亡率会随着年龄增长以及高血压、糖尿病、心血管疾病或慢性阻塞性肺疾病等合并症的存在而增加。新出现的证据表明，COVID-19会劫持免疫细胞的线粒体，在线粒体结构内复制，并损害线粒体动力学，导致细胞死亡。线粒体是细胞的动力源，在很大程度上参与维持细胞免疫、体内平衡以及细胞存活/死亡。越来越多的证据表明，受COVID-19感染的细胞中的线粒体非常脆弱，且脆弱性会随着年龄增长而增加。我们文章的目的是总结糖尿病、肥胖症和神经疾病等各种与年龄相关的合并症在增加COVID-19老年患者死亡率方面所起的作用。我们的文章还强调了冠状病毒与免疫细胞中线粒体动力学之间的相互作用。我们还强调了有助于预防COVID-19的当前治疗方法、生活方式和安全措施。迫切需要进一步研究以了解COVID-19患者中线粒体病毒与疾病进展之间的分子机制。
