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SARS-CoV-2 Infection Affects Mitochondrial Function, Study Finds

A new study suggests that therapies that boost mitochondrial function could potentially alleviate symptoms of severe COVID-19. Building on previous work showing that SARS-CoV-2 binds to mitochondria proteins and possibly affects oxidative phosphorylation, glycolysis, and other metabolic processes, researchers from the Children's Hospital of Philadelphia and elsewhere analyzed mitochondrial gene expression of about 700 nasopharyngeal samples from people with early-stage COVID-19 and 35 autopsy tissue samples from patients who had severe disease. As they report in Science Translational Medicine, the researchers found SARS-CoV-2 blocked the expression of oxidative phosphorylation-related mitochondrial genes while inducing glycolysis and immune responses in early-stage disease. But while in late-stage disease the virus was largely cleared and the expression of mitochondrial genes appeared to return to normal in the lungs, mitochondrial genes remained affected in other organs like the heart, liver, and kidneys. In animal models, the researchers further confirmed this pattern, but also noted effects in the brain. "Therapies that enhance mitochondrial function, minimize mROS, and block mtDNA release potentially could reduce the more severe symptoms of acute SARS-CoV-2 infection and mitigate the symptoms of long COVID," the researchers say.