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Remdesivir increases mtDNA copy number causing mild alterations to oxidative phosphorylation
Nicole DeFoor1, Swagatika Paul2, Shuang Li3
1School of Neuroscience, Virginia Tech, Life Science I Room 217, 970 Washington Street SW, Blacksburg, VA, 24061, USA.
Scientific Reports
|September 15, 2023
Summary
Remdesivir (RDV) treatment for COVID-19 showed increased mitochondrial DNA copy number in cells and liver but caused only mild functional changes. Skeletal muscle and heart tissues were notably resistant to RDV effects.
Area of Science:
- Virology
- Biochemistry
- Toxicology
Background:
- SARS-CoV-2 infection leads to COVID-19, treated with Remdesivir (RDV).
- RDV is an adenosine analogue that inhibits viral RNA transcription.
- Concerns exist regarding nucleoside analogues' potential mitochondrial toxicity.
Purpose of the Study:
- To investigate the effects of Remdesivir on mitochondrial function.
- To assess potential mitochondrial DNA (mtDNA) alterations induced by RDV.
Main Methods:
- In vitro studies using Mv1Lu cells.
- In vivo studies using rodent models.
- Analysis of mtDNA copy number and mitochondrial function.
Main Results:
- RDV treatment increased mtDNA copy number in Mv1Lu cells (35.26%) and rodent liver (100.27%).
- These increases were associated with only mild changes in overall mitochondrial function.
- Skeletal muscle and heart tissues demonstrated significant resistance to RDV treatment.
Conclusions:
- Remdesivir does not appear to significantly impair mitochondrial function.
- RDV's effects on mitochondria are generally mild, even with increased mtDNA copy number.
- Findings offer insights for RDV use in patients with pre-existing mitochondrial diseases.
