Researchers at the University of Malta have identified a biological trigger behind the muscle weakness often seen in people who endure prolonged COVID-19 symptoms. The findings were published in Biochimica et Biophysica Acta (BBA), a respected journal that explores cellular and molecular processes in health and disease.
Many COVID-19 survivors report lingering fatigue, breathlessness, trouble concentrating, and reduced muscle strength months after infection. These long‑haul symptoms, sometimes called long COVID, can interfere with daily life and work, and they affect a broad range of ages in North America as well as Europe and beyond.
The Malta team used an experimental model based on fruit flies to study the disease mechanism. The SARS‑CoV‑2 virus is known to hijack the ACE2 receptor to gain entry into cells. Yet researchers wanted to know what happens after this receptor is affected. In a controlled setup that removed the virus but altered ACE2 signaling, the researchers observed fatigue‑like symptoms in the organisms, suggesting that changes at the ACE2 site can trigger downstream effects that influence muscle function and energy levels.
Upon closer examination of ACE2’s role, the scientists found disruptions in the communication pathway between nerves and muscles. Several essential molecules that nerves rely on to relay signals to muscles were compromised, culminating in reduced muscle responsiveness and endurance. This points to a broader mechanism where the body’s own signaling networks, not just the virus, can contribute to persistent weakness after infection.
According to the study authors, the ACE2 receptor on the cell surface can be a target not only for viral invasion but also for immune processes. In other conditions such as multiple sclerosis, immune activity can affect receptor function, which may help explain some of the chronic symptoms observed in long COVID patients. The researchers emphasize that these interactions may represent a converging point where infection and immune responses intersect to influence neuromuscular health.
Beyond the lab, clinicians and researchers are continuing to monitor how these molecular changes translate into patient experiences. The work underscores the importance of evaluating neuromuscular health in recovered patients and exploring therapies that support nerve-to-muscle communication and energy production. While this study provides a piece of the puzzle, it also highlights the need for comprehensive care strategies that address fatigue and functional decline in long COVID, including rehabilitation and targeted pharmacologic approaches. Ongoing investigations will determine whether interventions that stabilize ACE2 signaling or protect nerve‑muscle signaling can shorten recovery times for some patients. [Citation: University of Malta study, published in Biochimica et Biophysica Acta (BBA).]
As health authorities in North America and around the world anticipate shifts in the pandemic landscape, clinicians stress proactive monitoring for lingering symptoms in patients who have recovered from the acute infection. Early assessment and a multidisciplinary approach may help individuals regain strength and stamina, reduce fatigue, and improve overall quality of life after COVID‑19. Researchers are hopeful that a clearer understanding of ACE2‑related pathways will lead to practical treatments that stabilize neuromuscular signaling and support long‑term recovery across diverse populations.