Nikhil Prasad Fact checked by:Thailand Medical News Team Aug 30, 2026 43 minutes ago
A new scientific review suggests that damage to mitochondria—the structures that generate most of a cell’s usable energy—could be an important link between SARS-CoV-2 infection and the persistent fatigue, muscle weakness, cardiovascular problems, and neurological symptoms seen in post-COVID-19 condition, commonly called Long COVID.
Mitochondrial dysfunction may help explain the persistent fatigue, inflammation, muscle problems,
and neurological symptoms experienced by people with Long COVID.
The review was conducted by scientists from the Federal University of Pará (UFPA), including its Institute of Biological Sciences, Laboratory of Human and Medical Genetics, and Graduate Program in Genetics and Molecular Biology; the State University of Pará (UEPA), including its Center of Biological and Health Sciences, Laboratory of Infectious and Cardiopulmonary Diseases, Graduate Program in Parasitic Biology in the Amazon, and Long COVID Program; and the University of São Paulo (USP), Institute of Chemistry, Laboratory of Energy Metabolism, Brazil.
How SARS-CoV-2 Disrupts Cellular Power
Mitochondria produce about 90% of cellular ATP, making them particularly important in energy-demanding tissues such as the heart, skeletal muscles, and nervous system. The review describes evidence that SARS-CoV-2 can disturb mitochondrial membranes, increase reactive oxygen species, impair mitophagy—the removal of damaged mitochondria—and interfere with antiviral signaling.
This Thailand
Medical News report highlights a particularly important cycle: damaged mitochondria can release mitochondrial DNA and other danger signals into cells and circulation. These signals can activate inflammatory pathways, including TLR9, the NLRP3 inflammasome, and cGAS-STING signaling, potentially amplifying inflammation even as mitochondrial energy production becomes less efficient.
Findings Point to Persistent Energy Problems
The review brings together several findings that may help explain Long COVID. Studies of patients after infection have reported reduced mitochondrial ATP production in peripheral blood immune cells, altered use of fats and glucose, increased oxidative stress, and changes in proteins controlling mitochondrial fusion and fission.
Researchers also identified evidence of longer-lasting molecular disruption. One study reported 21 differently regulated mitochondrial proteins a year after initial infection. Other evidence showed suppression of oxidative phosphorylation genes during acute COVID-19, while altered gene activity was observed even after viral genomes were no longer detectable in some experimental or tissue settings.
These abnormalities could have wide effects. Reduced ATP production may contribute to persistent fatigue, exercise intolerance, and muscle weakness. In the cardiovascular system, mitochondrial dysfunction may promote inflammatory signaling, apoptosis, and injury to energy-hungry heart cells. In the nervous system, impaired mitochondrial function may contribute to oxidative stress, neuroinflammation, and symptoms including cognitive proble
ms, pain, and fatigue.
Genetics Could Influence Who Is Most Vulnerable
The review also examines mitochondrial DNA variants associated with severe COVID-19 and variants previously linked with neurological, muscular, and cardiac disorders. However, evidence directly connecting specific mitochondrial genetic variants to Long COVID remains scarce.
Conclusions
Overall, the evidence supports mitochondria as a potentially important biological crossroads connecting genetic susceptibility, disrupted immunity, chronic inflammation, and impaired energy metabolism after SARS-CoV-2 infection.
Larger longitudinal studies are still needed to determine which mitochondrial changes cause persistent symptoms, identify useful biomarkers, and establish whether therapies targeting mitochondrial function can safely improve Long COVID outcomes.
The study findings were published in the peer reviewed journal: Genetics and Molecular Biology.
https://www.scielo.br/j/gmb/a/cjNv4pwNPydrcQNtjF8mSVs/?lang=en
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https://www.thailandmedical.news/articles/long-covid
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