COVID-19 Mitochondria Damage is Behind Long COVID and the Increased Risk of Future Non-Communicable Diseases
Nikhil Prasad Fact checked by:Thailand Medical News Team Jul 04, 2025 7 hours, 6 minutes ago
Medical News: The Overlooked Culprit Behind Lingering Symptoms
Emerging scientific evidence is now pointing to a new root cause behind Long COVID and the growing wave of chronic health problems seen after COVID-19 infection — mitochondrial damage. According to a comprehensive study by researchers from the University of Copenhagen’s Department of Biomedical Sciences, the Copenhagen University Hospital – Amager and Hvidovre, and the University Hospital Herlev’s National Center for Cancer Immune Therapy, the SARS-CoV-2 virus impairs mitochondrial health in both the acute and post-acute stages of the illness. This
Medical News report highlights how these disruptions may drive long-term health consequences and increase the risk for non-communicable diseases (NCDs) such as heart disease, kidney dysfunction, and diabetes.
COVID-19 Mitochondria Damage is Behind Long COVID and the Increased Risk of Future
Non-Communicable Diseases
Understanding Mitochondria and Their Role in COVID-19
Mitochondria are the powerhouses of our cells, responsible for generating energy. But beyond energy production, they are also deeply involved in immune responses and cellular stress management. When SARS-CoV-2 enters the body, it hijacks these organelles, disrupting their normal function and triggering a cascade of immune responses. In both acute COVID-19 and Long COVID, mitochondria are observed to be structurally damaged and metabolically impaired, leading to reduced energy production and increased oxidative stress.
The virus not only causes this damage directly by infiltrating cells and associating with mitochondrial membranes but also indirectly through excessive inflammation. Inflammatory molecules like IL-6 and TNF-alpha — elevated during infection — are known to interfere with mitochondrial enzymes, damage mitochondrial DNA (mtDNA), and impair their ability to generate energy efficiently.
A Clear Link Between Mitochondrial Damage and Long COVID Symptoms
Researchers found evidence of persistent mitochondrial dysfunction in tissues from the lungs, heart, kidneys, and liver, even after the virus had been cleared. This dysfunction has been linked to symptoms such as extreme fatigue, breathlessness, and reduced exercise capacity — hallmark features of Long COVID. Studies showed that peripheral blood mononuclear cells (PBMCs) from Long COVID patients had significantly impaired mitochondrial respiration compared to healthy individuals.
Muscle biopsies from Long COVID patients also revealed abnormal mitochondrial shapes and lower energy output. Imbalances in proteins related to mitochondrial repair and recycling, like PINK1 and MFN2, were observed, indicating failed attempts by the body to fix or remove damaged mitochondria.
Why This Matters Beyond COVID-19
Mitochondrial dysfunction doesn’t just cause short-term symptoms. It has long-term health implications. Damaged mito
chondria release their contents, including mtDNA, into the bloodstream, which can trigger chronic inflammation. This inflammation, in turn, has been associated with organ damage and diseases like heart failure, chronic kidney disease, and even neurodegeneration.
The study also emphasized that even asymptomatic individuals post-COVID-19 showed signs of mitochondrial damage when compared to people who never contracted the virus, though the damage was more severe in those with Long COVID.
How SARS-CoV-2 Evades the Body’s Defense by Targeting Mitochondria
SARS-CoV-2 has developed clever strategies to suppress immune defenses by targeting mitochondria. It deploys several proteins (like ORF9b, ORF10, and NSP5) to weaken mitochondrial antiviral signaling (MAVS) and disrupt immune pathways such as the cGAS-STING axis. These tactics allow the virus to replicate more efficiently while further damaging mitochondrial health and prolonging inflammation.
A Dangerous Cycle of Damage and Disease
In COVID-19 patients, especially those with severe illness or prolonged symptoms, this combination of mitochondrial damage and chronic inflammation can spiral into long-term disease. The study highlights how mitochondrial dysfunction in COVID-19 is linked to the same biological pathways involved in kidney injury, cardiovascular disease, and respiratory disorders. Damaged mitochondria leaking DNA into the cytosol activate immune responses that may persist long after the virus is gone, causing tissue damage and scarring.
This creates a vicious cycle: the more mitochondrial damage, the more inflammation; and the more inflammation, the worse the damage to mitochondria and organs.
Conclusion: A Call for Mitochondria-Focused Research and Treatment
This research presents compelling evidence that mitochondrial dysfunction is not just a consequence of SARS-CoV-2 infection but a central driver of both acute symptoms and Long COVID. It also lays the foundation for understanding how the virus increases the risk of long-term non-communicable diseases. The findings suggest that therapies aimed at protecting or restoring mitochondrial health — such as antioxidants, metabolic regulators, or even gene-targeted treatments — may offer promising pathways for preventing or treating Long COVID.
Understanding the critical role of mitochondria offers a fresh lens to view post-COVID complications and future pandemic preparedness. As more data emerges, it becomes increasingly urgent to investigate how commonly used treatments during the acute phase of COVID-19 might affect mitochondrial health and either contribute to or help prevent long-term damage. This shift in focus could redefine how we treat viral infections, not just in the context of COVID-19, but for a wide range of future viral threats.
The study findings were published in the peer reviewed journal: npj Metabolic Health and Disease
https://www.nature.com/articles/s44324-024-00038-x
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https://www.thailandmedical.news/articles/coronavirus
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