New research paves the way for new strategies to address long-lasting COVID-19 complications.
Researchers at the University of Malta have identified a possible cause for the long-lasting and often debilitating symptoms faced by people with long-term chronic illnesses. COVID-19 (novel coronavirus infection).Recent research published in scientific journals Molecular basis of BBA disease This has implications for the development of medicines to treat individuals who have not fully recovered from COVID-19.
About 1 in 3 people who recover from COVID-19 experience disabling symptoms such as persistent fatigue, shortness of breath, “brain fog” (a term used to describe difficulty concentrating) and muscle weakness. continues to experience The origin of the long-lasting COVID-19 remains a mystery despite its growing global impact on everyday life.
SARS-CoV-2the coronavirus that causes the novel coronavirus disease (COVID-19), binds to the ACE2 (angiotensin-converting enzyme 2) receptor, which acts as a gateway to the infection pathway. virus infect cells. In a pioneering study, researchers at the University of Malta used fruit flies to suppress levels of the ACE2 receptor. In the absence of the virus, this was enough to cause fatigue and decreased exercise performance.
“Our study clearly shows that ACE2 depletion is central to the neuromuscular complications experienced by a significant proportion of COVID-19 patients,” said the University of Malta Motor Neuron Disease Research. Professor Reuben Couch, who leads the laboratory, said:
This compelling finding comes from a large-scale study that began during the heat wave of the pandemic and temporarily took over the lab’s primary focus in response to the global emergency. Professor Couch and his team have long used fruit flies to study ALS because of their striking genetic and biological similarity to humans.
Scientists in Malta analyzed molecular defects in organisms with downregulated ACE2 levels and found defective communication between nerves and muscles. It turns out that several key molecules that nerves need to send messages to muscles are compromised.
Various pathways are thought to coalesce to reduce ACE2 levels or reduce ACE2 function in humans after coronavirus infection. “The ACE2 receptor on the cell surface can not only be hijacked by the virus, but it can also be targeted by autoantibodies, allowing the immune system to attack the body, as it does in multiple sclerosis,” he said. Dr. Paul Herrera, who conducted the complex experiment, added. It was important for research. There are also reports of long-term persistence of the virus from initial infection.
A discovery by the University of Malta sheds light on the lasting effects of COVID-19 and paves the way for therapeutic approaches to alleviate the chronically disabling complications.
Reference: “Functional characterization of ACE2 orthologues” Drosophila “Providing Insights into Neuromuscular Complications of COVID-19,” Paul Herrera and Reuben J. Couch, 24 July 2023, Available here. Biochimica et Biophysica Acta (BBA) – molecular basis of disease.
DOI: 10.1016/j.bbadis.2023.166818
This research was funded by the Malta Science and Technology Council.