Transferrin identified as potential contributor to COVID-19 severity

Sam Wood
Could transferrin be a potential biomarker for COVID-19 severity?

The University of Kent’s School of Biosciences and the Institute of Medical Virology at Goethe-University, Frankfurt am Main, have identified that a glycoprotein known as transferrin may critically contribute to severe forms of COVID-19.

SARS-CoV-2 is the coronavirus that causes COVID-19. It is currently not known why some individuals develop only mild or no symptoms when infected, whilst others experience severe, life-threatening forms of the disease. However, it is known that the risk of COVID-19 becoming severe increases with age and is higher in males than in females. Many severe COVID-19 cases are characterised by increased blood clotting and thrombosis formation.

The team combined existing data on gene expression in humans and infected cells to search for molecules involved in blood coagulation that differ between females and males, change with age, and are regulated in response to SARS-CoV-2 infection.

Out of more than 200 candidate factors, researchers identified a glycoprotein called transferrin to be a procoagulant (a cause of blood clotting) that increases with age, is higher in males than in females, and is higher in SARS-CoV-2-infected cells. Hence, transferrin may have potential as a biomarker for the early identification of COVID-19 patients at high risk of severe disease.

Katie-May McLaughlin, the first author of the study said: ‘It is very exciting to be involved in such an important study that may improve therapies for COVID-19 in its most severe form’.

The study ‘COVID-19-related coagulopathy – Is transferrin a missing link? was published in the scientific journal Diagnostics.

The papers’ authors were:
University of Kent’s School of Biosciences
Katie-May McLaughlin, Stuart Masterson, Dr Mark Wass, Professor Martin Michaelis.
Goethe University Frankfurt’s Institute of Medical Virology
Marco Bechtel, Denisa Bojkova, Professor Sandra Ciesek, Professor Jindrich Cinatl.