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Research shows how SARS-CoV-2 virus can cause heart attack for a year after infection

While the damaging toxic effects of the Covid-19 causing SARS-CoV-2 virus on the various organs of the body is not unknown, scientists in University of Maryland, Baltimore, US, have now found the mechanism behind the toxic effect the virus has on the heart tissue that may cause heart attack or heart failure. 

Previous studies have confirmed that patients who got infected with the coronavirus ran the risk of heart tissue inflammation for at least a year after testing negative. Patients could develop inflammation of the heart tissue therefore leading to blood clot, abnormal heart rhythms, stroke, heart attack or heart failure. 

The findings, based on research with fruit flies and mouse heart cells, were published in Nature Communications Biology.

Although scientists have developed vaccines and medications to lessen the severity of Covid-19 disease, the therapies does not necessarily protect the heart or other organs from the damage that could be done by even a mild Covid-19 infection.

The scientists used a drug to reverse the toxic effects of the SARS-CoV-2 virus protein on the heart. The most toxic SARS-CoV-2 protein, according to a previous study is Nsp6. 

“Our research shows that individual SARS-CoV-2 proteins can each do major damage to specific tissues in the body — similar to what has been found for other viruses like HIV and Zika,” news agency PTI quoted senior author Zhe Han.

“To treat patients in the long run, we must first understand the mechanism behind what is causing the disease. By identifying these processes of injury in each tissue, we can test drugs to see whether any can reverse this damage; those drugs that show promise can then be further tested in clinical research studies,” Han said.

Last year, Han and his team identified the most toxic SARS-CoV-2 proteins in studies using fruit flies and human cells. They found a drug ‘selinexor’ reduced the toxicity of one of these proteins, but not the other one, known as Nsp6, according to the study.

Next, the study said, they found that the Nsp6 protein hijacked the fruit fly’s cells in its heart to turn on the glycolysis process, which enables cells to burn the sugar glucose for energy. Typically, heart cells use fatty acids as an energy source, but switch over to sugar metabolism during heart failure as these cells to try to repair the damaged tissue.

The researchers also found the Nsp6 protein did added damage by disrupting the cell’s powerhouse, called the mitochondria, which produces energy from sugar metabolism, according to the study.

The team then blocked sugar metabolism in fruit flies and mouse heart cells using the drug 2-deoxy-D-glucose (2DG). They found that the drug reduced the heart and mitochondria damage caused by the Nsp6 viral protein, the study said.

“So, we predict this drug that changes the metabolism in the heart back to what it was before infection would be bad for the virus, by both cutting off its energy supply and eliminating the pieces it needs to replicate,” Han said.

The researchers said that fortunately 2DG is inexpensive and is used regularly in laboratory research. Although 2DG has not been approved by the U.S. Food and Drug Administration to treat disease, the drug is currently in clinical trials for treatment of COVID-19 in India, the study said.

“With this research elucidating the pathways of the Nsp6 protein, we can refine the treatments we target for future research with the ultimate aim of reversing further heart damage in these patients.”

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