New research from the USC Leonard Davis School of Gerontology suggests that mitochondria are among the first defense lines against COVID-19 and identify critical differences in how SARS-CoV-2, the virus that causes COVID-19, affects mitochondrial genes when compared to other viruses.
These differences offer possible explanations as to why older adults and people with metabolic disfunction have more severe responses to COVID-19 than other individuals. They also provide a starting point for more targeted approaches that may help identify therapeutics, says senior author Pinchas Cohen, professor of gerontology, medicine, and biological sciences and dean of the USC Leonard Davis School.
“If you already have mitochondrial and metabolic dysfunction, then you may, as a result, have a low first line of defense against COVID-19.
Future work should consider mitochondrial biology as a primary intervention target for SARS-CoV-2 and other coronaviruses,” he said.
The study, published in the Nature journal Scientific Reports, expands on recent findings that COVID-19 mutes the body’s innate inflammatory response and reports that it does so by diverting mitochondrial genes from normal function.
“We already knew that our immune response was not mounting a successful defense to COVID-19, but we didn’t know why,” said Brendan Miller, a senior doctoral student at the USC Leonard Davis School.
Using the vast amounts of public data being uploaded in the early days of the virus outbreak, the restream performed RNA sequencing analyses that compared mitochondrial-COVID interactions to those of other viruses: respiratory syncytial virus, seasonal influenza A virus, and human parainfluenza virus 3. These reanalyses identified three ways COVID-19, but not the other viruses, mute the body’s cellular protective response.
“This study adds to a growing body of research on mitochondrial-COVID interactions and presents tissue and cell-specific effects that should be carefully considered in future experiments,” said Cohen.
