Canterbury/UK: A protein that may potentially contribute to severe forms of COVID-19 has recently been identified by the School of Biosciences and The University of Kent. institute of medical virology Feather Goethe University.
The study titled ‘A possible role of CD47-SIRPalpha axis in COVID-19 pathogenesis’ has been published by the scientific journal. current issues in molecular biology.
SARS-CoV-2 is the coronavirus that causes Covid-19. While many individuals develop only mild or no symptoms upon SARS-CoV-2 infection, others develop serious, life-threatening illnesses.
Researchers have found that infection of cells with SARS-CoV-2 increases the level of a protein called CD47 on the cell surface.
CD47 is a so-called “don’t eat me” signal to protect the immune system that protects cells from being destroyed. Virus-induced CD47 on the surface of infected cells is likely to protect them from recognition by the immune system, leading to the production of large amounts of virus, resulting in more severe disease.
Well-known risk factors for severe COVID-19 such as old age and diabetes are associated with higher CD47 levels. High CD47 levels also contribute to high blood pressure, which is a major risk factor for COVID-19 complications such as heart attack, stroke and kidney disease.
The data suggest that age and virus-induced high CD47 levels contribute to severe COVID-19 by preventing an effective immune response and increasing tissue and organ damage associated with the disease.
Since therapeutics targeting CD47 are in development, this discovery could result in improved COVID-19 treatments.
Professor Martin Michaelis from the University of Kent said, “This is exciting. We may have identified a key factor associated with severe COVID-19. This is a major step forward in tackling the disease and we are now looking forward to further advances in design.” of medical science.”
Professor Jindrich Sinatli, Goethe-University Frankfurtsaid, “These additional insights into the disease processes underlying COVID-19 may help us design better treatments, as well as provide an appreciation for the importance of the breadth of research being conducted. Through this avenue, We have achieved a great success and the example is that the fight against the disease continues.”
The study titled ‘A possible role of CD47-SIRPalpha axis in COVID-19 pathogenesis’ has been published by the scientific journal. current issues in molecular biology.
SARS-CoV-2 is the coronavirus that causes Covid-19. While many individuals develop only mild or no symptoms upon SARS-CoV-2 infection, others develop serious, life-threatening illnesses.
Researchers have found that infection of cells with SARS-CoV-2 increases the level of a protein called CD47 on the cell surface.
CD47 is a so-called “don’t eat me” signal to protect the immune system that protects cells from being destroyed. Virus-induced CD47 on the surface of infected cells is likely to protect them from recognition by the immune system, leading to the production of large amounts of virus, resulting in more severe disease.
Well-known risk factors for severe COVID-19 such as old age and diabetes are associated with higher CD47 levels. High CD47 levels also contribute to high blood pressure, which is a major risk factor for COVID-19 complications such as heart attack, stroke and kidney disease.
The data suggest that age and virus-induced high CD47 levels contribute to severe COVID-19 by preventing an effective immune response and increasing tissue and organ damage associated with the disease.
Since therapeutics targeting CD47 are in development, this discovery could result in improved COVID-19 treatments.
Professor Martin Michaelis from the University of Kent said, “This is exciting. We may have identified a key factor associated with severe COVID-19. This is a major step forward in tackling the disease and we are now looking forward to further advances in design.” of medical science.”
Professor Jindrich Sinatli, Goethe-University Frankfurtsaid, “These additional insights into the disease processes underlying COVID-19 may help us design better treatments, as well as provide an appreciation for the importance of the breadth of research being conducted. Through this avenue, We have achieved a great success and the example is that the fight against the disease continues.”
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