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Communication

COVID-19-Related Coagulopathy—Is Transferrin a Missing Link?

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School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK
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Institute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany
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Institute of Biochemistry II, Faculty of Medicine, Goethe University, 60590 Frankfurt am Main, Germany
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Frankfurt Cancer Institute, Goethe University, 60590 Frankfurt am Main, Germany
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Cardio-pulmonary Institute, Goethe University, 60590 Frankfurt am Main, Germany
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German Center for Infection Research, DZIF, External Partner Site, 60590 Frankfurt am Main, Germany
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Fraunhofer Institute for Molecular Biology and Applied Ecology (IME), Branch Translational Medicine und Pharmacology, 60590 Frankfurt am Main, Germany
*
Authors to whom correspondence should be addressed.
Diagnostics 2020, 10(8), 539; https://doi.org/10.3390/diagnostics10080539
Received: 13 July 2020 / Revised: 28 July 2020 / Accepted: 29 July 2020 / Published: 30 July 2020
(This article belongs to the Section Pathology and Molecular Diagnostics)
SARS-CoV-2 is the causative agent of COVID-19. Severe COVID-19 disease has been associated with disseminated intravascular coagulation and thrombosis, but the mechanisms underlying COVID-19-related coagulopathy remain unknown. The risk of severe COVID-19 disease is higher in males than in females and increases with age. To identify gene products that may contribute to COVID-19-related coagulopathy, we analyzed the expression of genes associated with the Gene Ontology (GO) term “blood coagulation” in the Genotype-Tissue Expression (GTEx) database and identified four procoagulants, whose expression is higher in males and increases with age (ADAMTS13, F11, HGFAC, KLKB1), and two anticoagulants, whose expression is higher in females and decreases with age (C1QTNF1, SERPINA5). However, the expression of none of these genes was regulated in a proteomics dataset of SARS-CoV-2-infected cells and none of the proteins have been identified as a binding partner of SARS-CoV-2 proteins. Hence, they may rather generally predispose individuals to thrombosis without directly contributing to COVID-19-related coagulopathy. In contrast, the expression of the procoagulant transferrin (not associated to the GO term “blood coagulation”) was higher in males, increased with age, and was upregulated upon SARS-CoV-2 infection. Hence, transferrin warrants further examination in ongoing clinic-pathological investigations. View Full-Text
Keywords: SARS-CoV-2; COVID-19; thrombosis; coagulation; coagulopathy; transferrin SARS-CoV-2; COVID-19; thrombosis; coagulation; coagulopathy; transferrin
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MDPI and ACS Style

McLaughlin, K.-M.; Bechtel, M.; Bojkova, D.; Münch, C.; Ciesek, S.; Wass, M.N.; Michaelis, M.; Cinatl, J., Jr. COVID-19-Related Coagulopathy—Is Transferrin a Missing Link? Diagnostics 2020, 10, 539. https://doi.org/10.3390/diagnostics10080539

AMA Style

McLaughlin K-M, Bechtel M, Bojkova D, Münch C, Ciesek S, Wass MN, Michaelis M, Cinatl J Jr.. COVID-19-Related Coagulopathy—Is Transferrin a Missing Link? Diagnostics. 2020; 10(8):539. https://doi.org/10.3390/diagnostics10080539

Chicago/Turabian Style

McLaughlin, Katie-May, Marco Bechtel, Denisa Bojkova, Christian Münch, Sandra Ciesek, Mark N. Wass, Martin Michaelis, and Jindrich Cinatl Jr. 2020. "COVID-19-Related Coagulopathy—Is Transferrin a Missing Link?" Diagnostics 10, no. 8: 539. https://doi.org/10.3390/diagnostics10080539

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