Long Covid’s muscle fatigue linked to depletion of ACE2 receptors

Muscular fatigue in long Covid patients has been linked to depletion of ACE2 receptors, which act as doorways for SARS-CoV-2 to infect cells and cause COVID-19, according to new research.

Curtailing ACE2 receptor levels in fruit flies was enough to induce fatigue and diminished mobility, in the absence of the Covid-causing virus, scientists at the University of Malta found.

”Our research clearly shows that depletion of ACE2 is central to the neuromuscular complications experienced by a significant percentage of COVID-19 patients,” said Ruben Cauchi, corresponding author of the study published in the journal Biochimica et Biophysica Acta.

Shedding light on the lasting impact of COVID-19, the research paved the way for therapeutic approaches to treat individuals not completely recovered from the infection, it said.

Upon analysing the fruit flies with reduced levels of ACE2 receptors, several key molecules required by nerves to send messages to muscles were found to have been compromised, the scientists observed.

This, they said, resulted in a breakdown in communication between nerves and muscles.

”In addition to being hijacked by the virus, the ACE2 receptor on the cell’s surface can also be targeted by autoantibodies (antibody acting against the human itself), with the immune system attacking the body as it does in Multiple Sclerosis,” said Paul Herrera, a study author.

Multiple Sclerosis is a chronic progressive nervous disorder in which the immune system attacks the layer protecting nerves and causes communication problems between the brain and the rest of the body.

They said that various pathways are thought to work together in bringing down ACE2 levels or dampen its function in humans following Covid infection.

Individuals suffering from long Covid are plagued by symptoms including lingering fatigue, breathlessness, brain fog and muscle weakness.

Even as long Covid is increasingly becoming a global burden affecting everyday functioning, its cause remains elusive.