Transferrin is a glycosylated plasma and transport protein for iron with a molecular weight of 79.6 kDa that can bind two iron (FeIII) ions. It mediates iron transport in plasma between the gastrointestinal tract, iron storage organs as the liver and iron-consuming organs as the hemopoietic tissue. The synthesis of transferrin occurs primarily in the liver and in smaller quantities in the brain. Plasma levels are dependent on iron requirement and availability of iron in the body. (1)
Elevated concentrations can indicate iron deficiency, while low concentrations can occur due to inflammation, malignancy, malnutrition, or chronic liver disease. At normal levels, the determination of the transferrin saturation can be used to screen for hemochromatosis. (1)
By September 06, nearly 27 million cases and 900.000 deaths due to COVID-19 were reported to the WHO. (2) Although the disease is diagnosed almost equally in men and women, severe cases occur more often in men, with higher rates of hospitalization, severity, and mortality. The risk for severe cases of COVID-19 additionally increases with age. (3, 4)
As disseminated intravascular coagulation (DIC) is also associated with severity and outcome of COVID-19, (5) McLaughlin et al. focused on finding links between DIC, age, and gender. (6)
The authors analyzed different databases and found six genes that are involved in coagulation, expressed at different levels between men and women, and changing with age. When compared to the proteomics of SARS-CoV-2 infected cells, these genes showed no interaction or upregulation due to the novel virus. (6)
Finally, the analysis of the proteomics of infected cells revealed a SARS-CoV-2 related upregulation of transferrin that is elevated in males and increases with age. Transferrin seems not to interact with SARS-CoV-2 proteins, suggesting an upregulation in response to the infection. (6)
Most importantly, transferrin does not only function as an iron transporter protein. Transferrin inhibits antithrombin and potentiates the effects of thrombin and coagulation factor FXIIa by iron-independent mechanisms. These findings can be considered as a reason for hypercoagulability and DIC in COVID-19, and the function of transferrin should be further examined. (6,7)
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1. Burtis CA, Ashwood ER, Bruns DE, Tietz NW, editors. Tietz textbook of clinical chemistry and molecular diagnostics: with 12 color plates. 4. ed. St. Louis, Mo: Elsevier, Saunders; 2006.
2. Coronavirus disease (COVID-19) Weekly Epidemiological Update Data as received by WHO from national authorities, as of 10 am CEST 6 September 2020. World Health Organisation; 2020 Sep.
3. COVID-19 sex-disaggregated data tracker [Internet]. Global Health 5050. Available from: globalhealth5050.org/covid19/sex-disaggregated-data-tracker/
4. Gebhard C, Regitz-Zagrosek V, Neuhauser HK, Morgan R, Klein SL. Impact of sex and gender on COVID-19 outcomes in Europe. Biol Sex Differ. 2020;11:29.
5. Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost. 2020;18:844–7.
6. McLaughlin K-M, Bechtel M, Bojkova D, Münch C, Ciesek S, Wass MN, et al. COVID-19-Related Coagulopathy—Is Transferrin a Missing Link? Diagnostics. 2020;10:539.
7. Tang X, Zhang Z, Fang M, Han Y, Wang G, Wang S, et al. Transferrin plays a central role in coagulation balance by interacting with clotting factors. Cell Res. 2020;30:119–32.