Covid-19 causes long-term mitochondrial dysfunction in the heart and other organs, as research published in the journal “Science Translational Medicine” finds.

Mitochondria, the energy producers of our cells, can be negatively affected by the virus leading to dysfunction of many organs. The researchers, led by a team from the Children’s Hospital of Philadelphia and the International Covid-19 Research Group, found that mitochondrial function had recovered after recovery in the lungs, but not in the heart, kidneys and liver. In the heart in particular, mitochondrial function remained impaired. In addition, at the time when the viral load was at its peak in the lungs, suppressed expression of mitochondrial genes was found in the cerebellum, although no virus was observed in the brain.

The above findings are a possible explanation for the consequences of long-term (long) covid.

“This study gives us strong evidence that we should stop thinking about Covid-19 as -strictly- a disease of the upper respiratory tract and start to see it as a systemic disorder that affects multiple organs,” says one of the study’s authors and director of the Center for Mitochondrial and Epigenetic Medicine at the Children’s Hospital of Philadelphia, Douglas Wallace. He adds that “the continued dysfunction we observed suggests that mitochondrial dysfunction could cause long-term damage to the internal organs of these patients.”

However, the research team found a potential therapeutic target in the small molecule RNA 2392 (miR-2392), which was shown to regulate mitochondrial function in human tissue samples used in this study.

Earlier this year, the Gates Foundation provided funding to Dr. Wallace and the Center for Mitochondrial and Epigenetic Medicine for research on how variation in mitochondrial DNA between populations worldwide can affect mitochondrial function and thus individual susceptibility to Sars-Cov-2. According to the researcher, the evidence that the virus significantly affects the function of mitochondria supports the hypothesis that individual differences in mitochondrial function could be a factor in the severity of the manifestation of Covid-19 in each person.