Researchers have discovered how SARS-CoV-2 viral protein affects cardiac tissue

According to studies, the virus that causes COVID-19, SARS-CoV-2, has a protein that affects cardiac cells. The medicine was discovered to neutralise the protein’s harmful effects on the heart.
Their results, which were based on research conducted by the University of Maryland School of Medicine’s (UMSOM) Center for Precision Disease Modeling with fruit flies and mouse heart cells, were published in Communications Biology, a Nature publication, on September 30, 2022. In comparison to those who have not been infected with the virus, people who have been infected with COVID-19 have a significantly higher risk of developing inflammation of the heart muscle, abnormal heart rhythms, blood clots, stroke, heart attacks, and heart failure for at least a year after infection.

Although scientists created vaccinations and drugs to minimise the severity of COVID-19 illness, these treatments do not protect the heart or other organs from the harm that even a slight infection can cause.
“In order to cure patients in the long run, we must first understand the mechanism behind the sickness.” “Our findings show that individual SARS-CoV-2 proteins can cause significant damage to specific tissues in the body, similar to what has been discovered for other viruses such as HIV and Zika,” said senior author Zhe Han, PhD, Professor of Medicine and Director of the UMSOM Center for Precision Disease Modeling.

“By identifying these damaged mechanisms in each tissue, we can test medications to determine if any of them may reverse the damage; those treatments that show promise can then be explored further in clinical research trials.”
Dr. Han and his colleagues identified the most lethal SARS-CoV-2 proteins in fruit flies and human cells last year. They discovered that the promising medicine selinexor lowered the toxicity of one of these proteins, Nsp6, but not the other.
In their most recent investigation, scientists discovered that Nsp6 is the most lethal SARS-CoV-2 protein in the fly heart.

They discovered that the Nsp6 protein hijacked the fruit fly’s heart cells to activate the glycolysis process, which allows cells to burn the sugar glucose for energy. Normally, heart cells use fatty acids as an energy source, however with heart failure, these cells convert to sugar metabolism in order to heal the damaged tissue. The Nsp6 protein also caused further harm by interfering with the cell’s powerhouse, the mitochondria, which creates energy from sugar metabolism.
The researchers next used the chemical 2-deoxy-D-glucose to inhibit sugar metabolism in fruit flies and mouse cardiac cells (2DG). They discovered that the medication minimised the damage produced by the Nsp6 viral protein to the heart and mitochondria.

“We know that certain viruses hijack the afflicted animal’s cell machinery to modify its metabolism in order to steal the cell’s energy supply, so we assume SARS-CoV-2 does something similar,” Dr. Han said. “Viruses may also use byproducts of sugar metabolism as building blocks to manufacture other viruses.” “So, we expect that this medicine, which restores the heart’s metabolism to pre-infection levels, will be harmful to the virus by cutting off its energy source and destroying the parts it need to replicate.”

The researchers stated that, thankfully, 2DG is affordable and widely utilised in laboratory research. Although the US Food and Medicine Administration has not licenced 2DG for illness treatment, the drug is now being tested in India for the treatment of COVID-19.
“Too many Americans who have recovered from COVID end up with dangerous heart conditions weeks or months later, and we need to learn the fundamental reasons why this is happening,” said Mark T. Gladwin, MD, Vice President for Medical Affairs at the University of Maryland, Baltimore and the John Z. and Akiko K. Bowers Distinguished Professor and Dean, UMSOM.

“By identifying the Nsp6 protein’s pathways, we can modify the medicines we target for future study, with the ultimate goal of reversing additional cardiac damage in these individuals.”