Researchers have identified a specific protein in SARS-CoV-2 that damages heart tissue. They then used a drug to reverse the toxic effects of this protein on the heart.
The team’s findings were published in the journal Nature, based on research done on fruit flies and mouse heart cells at the University of Maryland School of Medicine’s Center for Micro Disease Modeling (UMSOM).
People with COVID-19 have a 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 did not have the virus previously.
While scientists are rapidly developing vaccines and drugs to reduce the severity of the Covid-19 disease, these treatments do not protect the heart or other organs from the damage that even a mild infection can cause. .
D., director of the Center for Micro Disease Modeling at the University of Maryland School of Medicine and professor of medicine. “In order to treat patients long-term, we first need to understand the mechanism underlying the cause of the disease,” said Chi Han. Our research shows that individual SARS-CoV-2 proteins can cause significant damage to certain tissues in the body – similar to those found in other viruses such as HIV and Zika.”
“By identifying these damage processes in each tissue, we can test drugs to see if there are any drugs that can reverse this damage, and promising drugs can be tested in clinical trials. research.”
Last year, Dr. Han 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 found another protein known as Nsp6, which turns out to be the most toxic SARS-CoV-2 protein in the heart of the fly.
Next, they found that the Nsp6 protein hijacks Drosophila cells in their nuclei to enable the process of glycolysis, which allows the cells to burn glucose for energy.
Heart cells normally use fatty acids as an energy source, but during heart failure, these cells metabolize sugar as they try to repair damaged tissue.
The researchers also discovered that Nsp6 causes further damage by disrupting the cells’ powerhouses called mitochondria, which produce energy from sugar metabolism.
The team blocked sugar metabolism in fruit flies and rat heart cells using the drug 2-deoxy-D-glucose (2DG). They found that the drug reduced heart and mitochondrial damage caused by the viral protein Nsp6.
Dr Han said: “We know that some viruses hijack the mechanism of the cells of an infected animal to change its metabolism to steal the cell’s energy source, so we suspect that SARS-CoV-2 is doing a similar thing. Viruses also contain byproducts of sugar metabolism. Therefore, we expect that this drug, which restores the heart’s metabolism to the way it was before the infection, harms the virus by cutting off its energy source and removing the parts it needs to replicate.”
Source: Medical Express
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