Long COVID Study Reveals Genetic Damage to Mitochondria
A new study on long COVID has shed light on the genetic damage caused to mitochondria, which could help explain the lingering symptoms experienced by many individuals recovering from the virus. According to researchers from the Children’s Hospital of Philadelphia (CHOP) and the COVID-19 International Research Team (COV-IRT), the virus affects the mitochondria in cells, leading to malfunctions that result in serious complications, including organ failure.
Mitochondria are tiny organelles found in every living cell in our bodies. They play a crucial role in generating the energy needed for cell functioning. The genes responsible for mitochondria are located within the DNA in the main cell body, as well as within the mitochondria organelles themselves. The study found that COVID-19 proteins bind to mitochondrial proteins, leading to malfunctions in their normal functioning.
Autopsies conducted at CHOP revealed that while the lungs were able to recover from the mitochondrial damage caused by COVID-19, other vital organs such as the heart, kidneys, and liver exhibited malfunctions in their mitochondrial function. Even in cases where the virus was not detected in the brain tissue, long COVID showed suppressed mitochondrial function in the cerebellum.
The findings of this study provide valuable insights into the underlying causes of long COVID symptoms. It appears that the virus’s impact on mitochondria could explain the wide range of symptoms experienced by long COVID sufferers. These can include heart, kidney, and circulatory problems, lung complications, sleep disruptions, anxiety, muscle pain, and issues with the nervous and connective tissues, as well as digestive and respiratory symptoms.
It is worth noting that previous studies conducted over the past two years have already identified immune cell abnormalities and persistent blood clots in individuals recovering from COVID-19. An Australian study demonstrated signs of inflammation associated with abnormal circulation, while an Italian study revealed damage to cells associated with blood flow in long COVID patients.
The research also suggests that the symptoms of long COVID were more prevalent prior to the emergence of the Omicron variant and in individuals who had not been vaccinated. Those who contracted the virus again during the Omicron era were found to be more susceptible to long COVID.
Dr. Andrea Foulkes from Massachusetts General Hospital, who has been a senior researcher at the National Institutes of Health (NIH), stated that long COVID is not just a single syndrome but rather a collection of syndromes. The symptoms can vary greatly among individuals, including dry mouth, weakness, headaches, tremors, muscle and abdominal pain, fever, sweats, chills, and sleep disturbances.
This latest research adds to our understanding of the long-term effects of COVID-19 and highlights the importance of addressing mitochondrial damage in the development of treatments for long COVID. By identifying and targeting the mitochondrial malfunctions, researchers hope to alleviate the persistent symptoms experienced by those affected by long COVID.
As scientists continue to uncover the complexities of long COVID, further research is needed to develop effective strategies for prevention, diagnosis, and treatment. Understanding the genetic damage to mitochondria caused by the virus opens up new possibilities for targeted therapies that could significantly improve the quality of life for long COVID patients.
