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Home ยป Mitochondrial Damage in Multiple Organs Linked to Long COVID – MazMessenger
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Mitochondrial Damage in Multiple Organs Linked to Long COVID – MazMessenger

Robert GillBy Robert GillAugust 12, 2023No Comments2 Mins Read
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New Study Finds COVID-19 Impacts Mitochondrial Genes, Leading to Organ Dysfunction

Researchers from Children’s Hospital of Philadelphia (CHOP) and the Center for Organ Virology and Inflammation Research (COV-IRT) have led a consortium that recently made a groundbreaking discovery regarding the SARS-CoV-2 virus and its impact on mitochondrial genes. The study, published in Science Translational Medicine, reveals that the virus negatively affects these genes, resulting in dysfunction in various organs beyond just the lungs.

The team of researchers conducted a thorough analysis of nasal and autopsy tissue samples obtained from COVID-19 patients, as well as animal models, to better understand how the virus affects mitochondrial gene expression. The study found that the virus not only blocked the transcription of specific mitochondrial genes but also activated the host’s immune defenses.

One significant finding from the study is that mitochondrial gene expression recovered in the lungs but remained suppressed in other vital organs, including the heart, kidneys, and liver, as observed in the autopsy tissue samples. Surprisingly, in animal models, mitochondrial gene expression was suppressed in the cerebellum, despite the absence of the SARS-CoV-2 virus in the brain.

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These findings challenge the traditional perception of COVID-19 as solely an upper respiratory disease. The researchers suggest that it should be recognized as a systemic disorder that affects multiple organs.

Moreover, the study identified a potential therapeutic target in microRNA 2392, a molecule found to regulate mitochondrial function. By neutralizing this microRNA, it may be possible to hinder the replication of the virus and provide an additional treatment option that could mitigate severe complications in at-risk patients.

The research also supports the hypothesis that differences in individual mitochondrial function may contribute to the severity of COVID-19. Understanding these variances could aid in the development of personalized treatment strategies tailored to patients’ specific needs.

Based on these findings, the consortium of researchers emphasizes the need for exploring different approaches to treating COVID-19 beyond the conventional focus on respiratory symptoms. By targeting the impact of the virus on mitochondrial genes, new therapeutic options could emerge, potentially leading to more effective treatments for patients.

Robert Gill
Robert Gill
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Robert Gill

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