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Unmasking the Long COVID Mystery: New Study Reveals Cause of Muscle Weakness
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Around one in three individuals who recover from COVID-19 continue to experience life-disrupting symptoms, such as persistent fatigue, shortness of breath, ‘brain fog’ (a term used to describe concentration difficulties), and muscle weakness. The origin of long COVID, despite its increasing global impact on daily life, has remained a mystery.

SARS-CoV-2, the coronavirus responsible for COVID-19, latches onto the ACE2 (angiotensin-converting enzyme 2) receptor, which acts as the doorway through which the virus infects cells. In a pioneering study, researchers at the University of Malta exploited fruit flies to curb down the levels of the ACE2 receptor. In the absence of the virus, this was enough to induce fatigue and diminished mobility.

“Our research clearly shows that depletion of ACE2 is central to the neuromuscular complications experienced by a significant percentage of COVID-19 patients,” said Professor Ruben Cauchi, who heads the Motor Neuron Disease Laboratory at the University of Malta.
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When analyzing molecular defects in organisms with downregulated ACE2 levels, the Maltese scientists discovered a breakdown in communication between nerves and muscles. Several key molecules required for nerves to send messages to muscles were found compromised.

Various paths are thought to coalesce to bring down ACE2 levels or dampen its function in humans following a coronavirus infection. “In addition to being hijacked by the virus, the ACE2 receptor on the cell’s surface can also be targeted by autoantibodies, with the immune system attacking the body as it does in Multiple Sclerosis,” added Dr. Paul Herrera, who performed the intricate experiments that were crucial to the study. There have also been reports of virus persistence long after the initial infection.
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