Is mitochondrial dysfunction behind long Covid?

Scientists are looking into how mitochondria, known as the body’s power plants, fueling our cells, could be the key to unlocking treatments for long Covid.

Long Covid is defined as having new or ongoing symptoms four weeks or more after the start of disease. Symptoms include fatigue, shortness of breath, loss of concentration and joint pain. The symptoms can adversely affect day-to-day activities, and in some cases can be severely limiting.

Betty Raman, cardiologist at Oxford University is running a clinical trial investigating a potential treatment for the fatigue and muscle weakness experienced by many patients suffering long-term effects from the Covid virus, the Guardian reported.

According to Raman, it is widely recognised that mitochondrial dysfunction may contribute to the profound fatigue associated with long Covid.

In the trial, she aims to explore whether an amino acid cocktail known as AXA1125, produced by US-based biotech Axcella Therapeutics, can help long Covid patients fight fatigue.

“The drug is a powdered drink, consumed three times a day along with meals, and we’re hoping that it will help people with their energy levels and fatigue,” Raman was quoted as saying.

“The idea is that it can give the mitochondria additional fuel to produce energy, and help repair damaged mitochondria. Hopefully, by the end of July, we should have some top line results to report,” she added.

Previous research conducted by Raman and others on fatigued patients post Covid infection, with no obvious heart or lung abnormalities, led to the notion that mitochondria may be involved. This symptom is often referred to as post-exertional malaise (PEM), and is also experienced by people with genetic mitochondrial diseases.

Further, in long Covid patients with PEM, Raman found that their muscles struggle to extract oxygen from the blood as efficiently as might be expected.

In addition, a research published in Chronic Diseases and Translational Medicine showed that mitochondria in white blood cells were not as efficient in generating ATP, a complex chemical that acts as a form of energy currency for cells, in patients recovering from Covid-19. Mitochondria is known to convert the food we eat into ATP.

According to David Systrom, a pulmonary and critical care doctor at Brigham & Women’s Hospital, Boston, abnormalities at the electron level, deep within the mitochondria may explain the reason why the mitochondria of long Covid patients become sluggish in generating ATP, the report said.

Systrom found the answers through studying patients with chronic fatigue syndrome, also known as ME/CFS, an illness that bears many similarities to long Covid.

Systrom is now running his own clinical trial in both ME/CFS and long Covid patients, in partnership with Japanese drug company Astellas, which has developed a drug that aims to restore normal mitochondrial metabolism.

Both Raman and Systrom agree that mitochondrial dysfunction is only likely to be a factor in a subset of long Covid and ME/CFS patients, the report said.

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