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Updated: Sep 14, 2025
08:48
Author Spotlight: Decoding Mitochondrial Aging
Published on: June 30, 2023
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Viral mitochondriopathy in COVID-19
Tsung-Hsien Chen1, Tien-Hsin Jeng2, Ming-Yang Lee3
1Department of Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chiayi, 60002, Taiwan.
Redox Biology
|July 18, 2025
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disrupts mitochondria, causing inflammation and organ dysfunction in COVID-19 and long COVID. This review explores SARS-CoV-2
Area of Science:
- Mitochondrial biology
- Virology
- Immunology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to multi-organ dysfunction.
- Mitochondrial dysfunction is implicated in the pathogenesis of COVID-19 and long COVID.
Purpose of the Study:
- To review current findings on how SARS-CoV-2 impacts cellular mitochondria.
- To examine the role of mitochondrial disruption in chronic inflammation and long-term health risks.
- To discuss potential therapeutic strategies targeting mitochondrial dysfunction.
Main Methods:
- Literature review of recent studies on SARS-CoV-2 and mitochondrial interactions.
- Analysis of viral mechanisms affecting mitochondrial function and antiviral responses.
Main Results:
- SARS-CoV-2 proteins induce mitochondrial bioenergetic collapse and disrupt mitochondrial dynamics.
- Viral infection impairs mitochondrial ionic homeostasis and evades innate antiviral defenses.
- Mitochondrial damage contributes to both acute COVID-19 symptoms and long COVID sequelae.
Conclusions:
- Mitochondrial dysfunction is a key mechanism underlying COVID-19 pathogenesis and chronic sequelae.
- Understanding these mechanisms is crucial for developing effective treatments for COVID-19 and long COVID.
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