Protein Called CD47 Found On Cell Surfaces Found To Be Contributing Factor To COVID-19 Disease Severity According To Study By UK and German Scientists
: A new study led by researchers from University of Kent-UK and Goethe University-Germany has discovered that a protein that is a component of the human immune system called CD47, found on cell surfaces plays a contributing factor to COVID-19 disease severity.
Typically most SARS-CoV-2 infections are mild or even asymptomatic. However, a small fraction of infected individuals develops severe, life-threatening disease, which is caused by an uncontrolled immune response resulting in hyperinflammation. However, the factors predisposing individuals to severe disease remain poorly understood.
The study team shows that levels of CD47, which is known to mediate immune escape in cancer and virus-infected cells, are elevated in SARS-CoV-2-infected Caco-2 cells, Calu-3 cells, and air−liquid interface cultures of primary human bronchial epithelial cells.
Moreover, SARS-CoV-2 infection increases SIRPalpha levels, the binding partner of CD47, on primary human monocytes. Systematic literature searches further indicated that known risk factors such as older age and diabetes are associated with increased CD47 levels. High CD47 levels contribute to vascular disease, vasoconstriction, and hypertension, conditions that may predispose SARS-CoV-2-infected individuals to COVID-19-related complications such as pulmonary hypertension, lung fibrosis, myocardial injury, stroke, and acute kidney injury.
Hence, age-related and virus-induced CD47 expression is a candidate mechanism potentially contributing to severe COVID-19, as well as a therapeutic target, which may be addressed by antibodies and small molecules. Further research will be needed to investigate the potential involvement of CD47 and SIRPalpha in COVID-19 pathology. The study findings should encourage other research groups to consider the potential relevance of the CD47/ SIRPalpha axis in their COVID-19 research.
The study findings were published in the peer reviewed journal: Molecular Biology. https://www.mdpi.com/1467-3045/43/3/86/htm
The study team identified the protein CD47 that may critically contribute to severe forms of COVID-19.
Although most people with COVID-19 disease develop only mild or no symptoms upon SARS-CoV-2 infection, others develop severe, life-threatening disease.
The COVID-19 Research
team had found that the infection of cells with SARS-CoV-2 results in increased levels of a protein called CD47 on the cell surface.
Interestingly CD47 is a so-called 'do not eat me' signal to the immune system's defenses that protect cells from being destroyed. Virus-induced CD47 on the surface of infected cells is likely to protect them from immune system recognition, enabling the production of larger amounts of virus, resulting in more severe disease.
It was found that well-known risk factors for severe COVID-19 such as older age and diabetes are associated with higher CD47 levels. High CD47 levels also contribute to high blood pressure, which is a large risk factor for COVID-19 complications such as heart attack, stroke, and kidney disease.
The study findings suggest that age and virus-induced high CD47 levels contribute to severe COVID-19 by preventing an effective immune response and increasing disease-associated tissue and organ damage.
As therapeutics targeting CD47 are already in development, this discovery may result in improved COVID-19 therapies.
Co-corresponding author, Dr Martin Michaelis, a professor at the School of Biosciences, University of Kent told Thailand Medical News, "This is exciting. We may have identified a major factor associated with severe COVID-19. This is a huge step in combatting the disease and we can now look forward to further progress in the design of therapeutics."
Dr Jindrich Cinatl, a professor from the Institute for Medical Virology, Goethe University and also a co-corresponding author added, "These additional insights into the disease processes underlying COVID-19 may help us to design better therapies, as well as appreciation for the importance of the breadth of research being conducted. Through this avenue, we have achieved a major breakthrough and exemplified that the fight against the disease continues."
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