COVID-19 Causes mtDNA Mutations and Alters Oxidative Phosphorylation Genes Leading to Mitochondrial Dysfunction
Nikhil Prasad Fact checked by:Thailand Medical News Team Nov 18, 2024 1 month, 12 hours, 22 minutes ago
Medical News: The fight against COVID-19 continues to unravel hidden facets of how the virus wreaks havoc in the human body. Recent research spearheaded by scientists from the University of Sistan and Baluchestan and Zahedan University of Medical Sciences in Iran has unveiled a groundbreaking link between the virus and mitochondrial dysfunction. Their study dives into the effects of mitochondrial DNA (mtDNA) mutations and altered oxidative phosphorylation (OXPHOS) gene expression on the severity of COVID-19 infections.
COVID-19 Causes mtDNA Mutations and Alters Oxidative Phosphorylation Genes
Leading to Mitochondrial Dysfunction
Decoding the Mitochondria-COVID-19 Connection
Mitochondria are the powerhouse of cells, responsible for generating energy and maintaining cellular health. Their genetic material, mtDNA, encodes critical components of the energy production system, specifically the OXPHOS pathway. When SARS-CoV-2, the virus behind COVID-19, infiltrates the body, it not only triggers respiratory symptoms but also disrupts mitochondrial functions.
This
Medical News report explores findings from the study involving 50 individuals - 30 COVID-19 patients and 20 healthy controls. Researchers utilized advanced genomic sequencing to identify mtDNA mutations and analyzed their impact on protein structure and stability. They further examined the expression levels of 13 key mitochondrial genes linked to OXPHOS.
What the Research Revealed
The study discovered eight distinct mtDNA mutations across ND1, ND5, CO3, ATP6, and CYB genes in COVID-19 patients. Among these, two unique mutations stood out: C9555T in the CO3 gene and A12418T in the ND5 gene. These mutations were predicted to destabilize mitochondrial proteins, impairing their functionality. Notably, the downregulation of key mitochondrial genes correlated with clinical markers such as increased white blood cells (WBC), liver enzyme levels, and disease severity.
Gene expression analysis revealed that mitochondrial genes across four complexes - Complex I (ND genes), Complex III (CYB), Complex IV (CO genes), and Complex V (ATP genes) - were significantly downregulated in COVID-19 patients compared to healthy controls. This reduction indicates compromised mitochondrial energy production, which exacerbates the body’s ability to cope with the infection.
Implications of Mitochondrial Dysfunction
The identified mtDNA mutations are linked to reduced protein stability and functionality, leading to mitochondrial respiratory chain defects. Such dysfunctions manifest as increased oxidative stress, reduced ATP production, and heightened inflammatory responses. This sets the stage for severe COVID-19 outcomes, including multi-organ failure.
One key finding is the role of Complex I and IV mutations in disrupting mitochondrial processes. These mutations can lead to excessive production of reactive oxygen species (ROS), a hallmark of oxidative stress, further amplifying cellular d
amage.
Clinical and Laboratory Correlations
The study observed significant clinical correlations between mtDNA changes and patient outcomes. COVID-19 patients exhibited elevated markers like leukocytes, neutrophils, creatinine, and liver enzymes (ALT and AST). Conversely, oxygen saturation (SpO2), hemoglobin, and red blood cell counts were markedly reduced.
Mitochondrial gene expression levels also showed strong associations with laboratory markers. For example, the expression of CO3, ND2, and ATP6 genes significantly correlated with SpO2 and inflammatory markers. These insights suggest that mtDNA alterations could serve as diagnostic or prognostic biomarkers for COVID-19.
Broader Impacts and Future Directions
The findings underscore the potential of targeting mitochondrial dysfunction as a therapeutic strategy for COVID-19. Interventions aimed at stabilizing mitochondrial functions or reducing oxidative stress might mitigate disease severity. Moreover, understanding the role of mtDNA mutations could pave the way for personalized treatments based on an individual's genetic susceptibility to mitochondrial damage.
Conclusion
This research highlights the critical role of mitochondrial integrity in determining the severity of COVID-19 infections. By disrupting mtDNA and OXPHOS pathways, the virus weakens cellular defenses and heightens inflammatory responses, leading to severe disease outcomes. The study not only provides a new lens to understand COVID-19 pathogenesis but also opens avenues for targeted therapies.
The study findings were published in the peer-reviewed Iranian Journal of Allergy, Asthma, and Immunology.
https://publish.kne-publishing.com/index.php/IJAAI/article/view/16212’
https://ijaai.tums.ac.ir/index.php/ijaai/article/view/4051
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https://www.thailandmedical.news/news/new-insights-into-mitochondrial-role-in-post-covid-recovery-and-long-covid-progression
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