Severity of COVID-19 illness may depend on levels of one protein

CANTERBURY, England — One protein which scientists say sends out the “do not eat me” signal to the human immune system may be responsible for people having more severe cases of COVID-19. Researchers from the University of Kent have discovered that higher levels of this protein on the surface of infected cells may be blocking the immune system from doing its job.

Although many patients infected with SARS-CoV-2, the virus causing COVID-19, will only develop mild symptoms, others will experience severe and life-threatening reactions. COVID-19 is already responsible for nearly 700,000 deaths in the United States. The new findings reveal that the protein CD47 may play a major role in these deaths.

Protein discovery is ‘huge step’ in beating COVID

CD47 sends out a signal that prevents the immune system’s defenses from accidentally destroying healthy cells. However, researchers found that when SARS-CoV-2 infects human cells, more CD47 appears on the cell surface. The team adds this is likely keeping the immune system from recognizing the infected cells as a threat. Without the immune system attacking these cells, the virus can continue to replicate and lead to more severe symptoms.

Study authors add that specific risk factors for severe COVID-19 infections — like old age and pre-existing conditions such as diabetes — also show a link to higher CD47 protein levels. High CD47 levels contribute to high blood pressure as well — another risk factor for severe COVID complications.

Researchers note that therapeutics which target CD47 are already in development. Their findings may help to improve their effectiveness during the COVID-19 pandemic.

“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,” says Professor Martin Michaelis in a media release.

“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,” adds Professor Jindrich Cinatl from Goethe University-Frankfurt.

The study appears in the journal Current Issues in Molecular Biology.

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