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COVID-19

Do compromised mitochondria aggravate severity and fatality by SARS-CoV-2?

ORCID Icon & ORCID Icon
Pages 911-916 | Received 28 Jul 2021, Accepted 06 Apr 2022, Published online: 22 Apr 2022

Figures & data

Figure 1. A proposed model on the link between defective mitochondria regulated intracellular temperature and high severity of COVID-19. In the case of alveolar epithelial cells, defective mitochondria potentially are not able to contribute towards intracellular temperature. In fact, intracellular temperature is proposed to be lower compared to the alveolar epithelial cells with healthy and functional mitochondria.

Figure 1. A proposed model on the link between defective mitochondria regulated intracellular temperature and high severity of COVID-19. In the case of alveolar epithelial cells, defective mitochondria potentially are not able to contribute towards intracellular temperature. In fact, intracellular temperature is proposed to be lower compared to the alveolar epithelial cells with healthy and functional mitochondria.

Figure 2. A proposed model on the link between healthy mitochondria regulated intracellular temperature and less severity of COVID-19. Alveolar epithelial cells with healthy and functional mitochondria maintain slightly higher temperature than the alveolar epithelial cells with defective mitochondria. Here, the proposed model suggests that an optimal intracellular temperature of alveolar epithelial cells with good mitochondrial may not be a better intracellular environment for the replication and assembly of SARS-CoV-2 compared to alveolar epithelial cells harboring defective mitochondria.

Figure 2. A proposed model on the link between healthy mitochondria regulated intracellular temperature and less severity of COVID-19. Alveolar epithelial cells with healthy and functional mitochondria maintain slightly higher temperature than the alveolar epithelial cells with defective mitochondria. Here, the proposed model suggests that an optimal intracellular temperature of alveolar epithelial cells with good mitochondrial may not be a better intracellular environment for the replication and assembly of SARS-CoV-2 compared to alveolar epithelial cells harboring defective mitochondria.

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