Study shows how SARS-CoV-2 causes heart attack after infection

Researchers have identified a specific SARS-CoV-2 protein that damages heart tissue. They then used the drug to reverse the toxic effects of this protein on the heart.

The group’s findings are published by the University of Maryland School of Medicine’s Center for Microdisease Modeling (UMSOM), based on research on fruit flies and mouse heart cells, in the journal Nature.

People with COVID-19 are at significantly greater risk of developing myocarditis, arrhythmias, blood clots, stroke, heart attack, and heart failure for at least a year after infection compared to those who have not previously had the virus.

While scientists have rapidly developed vaccines and drugs to reduce the severity of Covid-19, these treatments do not protect the heart or other organs from the damage that even a mild infection can cause.

“In order to treat patients in the long term, we must first understand the mechanism underlying the cause of disease,” said lead researcher Dr. Chi Han, MD, professor of medicine and director of the Center for Microdisease Modeling at the University of Marylane School. Our study shows that individual SARS-CoV-2 proteins can cause significant damage to certain body tissues, similar to what has been found in other viruses such as HIV and Zika.”

“By identifying these damage processes in each tissue, we can test drugs to see if they can reverse this damage, and those drugs that seem promising can then be tested in clinical trials.”

Last year, Dr. Khan and his research team identified the most toxic SARS-CoV-2 protein in studies using fruit flies and human cells. They found a promising drug that reduces the toxicity of one of these proteins called selinexor.

Now, researchers have discovered another protein, known as Nsp6, that appears to be the most toxic SARS-CoV-2 protein in the fly’s heart.

They then discovered that the Nsp6 protein hijacks fruit fly cells in their nuclei to activate the glycolysis process, which allows the cells to burn glucose for energy.

Heart cells normally use fatty acids for energy, but in heart failure switch to sugar metabolism as these cells try to repair damaged tissue.

The researchers also found that Nsp6 does further damage by disrupting the cells’ powerhouse called mitochondria, which generate energy from sugar metabolism.

The team then blocked sugar metabolism in Drosophila and rat heart cells with the drug 2-deoxy-D-glucose (2DG). They found that the drug reduced damage to the heart and mitochondria caused by the viral Nsp6 protein.

Dr Khan said: “We know that some viruses hijack an infected animal’s cell machinery to change its metabolism and steal the cell’s energy source, so we suspect that SARS-CoV-2 is doing something similar. Viruses can also use the by-products of sugar metabolism as building blocks to create more viruses. So we expect this drug, which changes the heart’s metabolism to what it was before infection, would be detrimental to the virus by cutting off its energy supply and removing parts needed to replicate.”

Source: Medical Express

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