A drug developed by the Defense Research and Development Organization (DRDO) can cause damage to the opposite center caused by a protein in the SARS-CoV-2 virus, according to a study conducted on fruit flies and mice.
Researchers at the University of Maryland have discovered how a protein contained in SARS-CoV-2, the virus that causes COVID-19, damages central tissue. They then used the drug, called 2DG, to counteract the harmful effects of this protein at the center.
Developed through Dr. Reddy’s laboratories in collaboration with DRDO, 2DG is an oral drug. The SARS-CoV-2 virus on the glycolysis or breakdown of glucose for energy. The drug hinders the process of glycolysis and prevents the spread of the virus.
People inflamed with COVID-19 are at particularly higher risk for central muscle inflammation, heart rhythms, blood clots, strokes, central seizures, and central failure for at least a year after infection, compared to those who were not inflamed. inflamed with the virus, according to the study.
The scientists, who are from the University of Maryland, Baltimore, USA. In the U. S. , they then used a drug to counteract the poisonous effects of the SARS-CoV-2 virus protein on the heart.
“Our studies show that individual SARS-CoV-2 proteins can cause primary damage to the body’s expressive tissues, similar to what has been discovered for other viruses such as HIV and Zika,” said leader Zhe Han.
Their findings, on studies on fruit flies and mouse central cells, were published in the peer-reviewed journal Nature Communications Biology.
Although scientists around the world temporarily developed vaccines and drugs to mitigate the severity of COVID-19 disease, the study found that those treatments did not damage the center or other organs of damage that even a mild infection could cause.
“To treat patients long-term, we first want to perceive the mechanism that causes the disease. By identifying those injury processes in each tissue, we can check the drugs to see if some can counteract this damage; drugs that are promising can then be further verified in clinical study studies,” Han said.
Last year, Han and his team learned about SARS-CoV-2’s peak poisonous proteins in studies of fruit flies and human cells. According to the study, they found that a “selinexor” drug reduced the toxicity of one of those proteins, but not the other, known as Nsp6.
In their most recent study, they found that Nsp6 turned out to be the most poisonous SARS-CoV-2 protein in the fly heart.
Then, according to the study, they found that the Nsp6 protein hijacked fruit fly cells at its center to activate the glycolysis process, allowing cells to burn glucose sugar for energy. Usually, core cells use fatty acids as an energy source, however, they are transferred to the fault of the sugar metabolism center because those cells try to repair the broken tissue.
The researchers also found that the Nsp6 protein further damages by disrupting the cell’s nerve center, called mitochondria, which produces energy from sugar metabolism, according to the study.
The team then blocked sugar metabolism in fruit flies and mouse core cells with the drug 2-deoxy-D-glucose (2DG). They found that the drug reduced damage to the center and mitochondria caused by the viral protein Nsp6, according to the study.
“We know that some viruses hijack the cellular machinery of the inflamed animal to adjust its metabolism and tap into the cell’s energy source, so we suspect SARS-CoV-2 does something similar. Viruses can also use the byproducts of sugar metabolism as building blocks to make more viruses,” Han said.
“So we hope that this drug that returns the heart’s metabolism to what it was before infection will be bad for the virus, whether it’s cutting off its energy source and eliminating the portions it wants to replicate,” Han said.
The researchers said that, fortunately, 2DG is affordable and used in laboratory research. Although the U. S. Food and Drug Administration is not able to do so. UU. no the 2DG has been approved to treat the disease, the drug is lately in clinical trials for the treatment of COVID-19 in India, according to the study.
“Too many Americans who have recovered from COVID end up with a harmful central illness weeks or months later, and we want to be told the basic reasons why that happens,” Mark T said. Gladwin, vice president of medical affairs at the University of Maryland. . .
“With these studies elucidating the Nsp6 protein pathways, we can refine the remedies we target for long-term studies with the ultimate goal of reversing further central damage in those patients. “
(This story has not been edited through NDTV and is automatically generated from a syndicated source. )
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