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<p>Arterial and venous thrombosis, atrial fibrillation, and viral myocarditis are potentially life-threatening conditions and well-documented complications of both COVID-19 and influenza. Therefore, clinicians should be aware of all factors that may promote their occurrence, particularly those related to common viral infections such as influenza and SARS-CoV-2. Both influenza and SARS-CoV-2 utilize transferrin receptor 1 (TfR1) to enter host cells; notably, SARS-CoV-2 has been detected in tissues that do not express ACE2. TfR1 is highly expressed on cardiomyocytes, as well as on endothelial cells. Iron deficiency —a common disorder in the general population- promotes overexpression of TfR1, thereby facilitating the entry of SARS-CoV-2 and influenza viruses into cardiomyocytes and endothelial cells. Therefore, an increased expression of the TfR1 on cardiomyocytes may consequently contribute to the development of viral myocarditis, and atrial fibrillation. Finally, TfR1 is involved in viral uptake by endothelial cells and in molecular pathways implicated in thrombus formation. Clinicians should recognize that individuals with iron deficiency and concomitant SARS-CoV-2 or influenza infection may be at increased risk of arterial and venous thrombosis, atrial fibrillation, and viral myocarditis. Given that approximately two billion people worldwide have some degree of iron deficiency—especially older adults and young children—appropriate preventive strategies should be considered.</p> Graphical Abstract <p></p>

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Iron Deficiency as an Important Predictor of Arterial and Venous Thrombosis, Myocarditis, and Atrial Fibrillation in COVID-19 and Influenza

  • 期刊论文

  • 发表日期：

    2026年5月19日

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  • Ana Cirovic,
  • Nemanja Brankovic,
  • Gorjana Antelj,
  • Aleksandar Cirovic

摘要

Arterial and venous thrombosis, atrial fibrillation, and viral myocarditis are potentially life-threatening conditions and well-documented complications of both COVID-19 and influenza. Therefore, clinicians should be aware of all factors that may promote their occurrence, particularly those related to common viral infections such as influenza and SARS-CoV-2. Both influenza and SARS-CoV-2 utilize transferrin receptor 1 (TfR1) to enter host cells; notably, SARS-CoV-2 has been detected in tissues that do not express ACE2. TfR1 is highly expressed on cardiomyocytes, as well as on endothelial cells. Iron deficiency —a common disorder in the general population- promotes overexpression of TfR1, thereby facilitating the entry of SARS-CoV-2 and influenza viruses into cardiomyocytes and endothelial cells. Therefore, an increased expression of the TfR1 on cardiomyocytes may consequently contribute to the development of viral myocarditis, and atrial fibrillation. Finally, TfR1 is involved in viral uptake by endothelial cells and in molecular pathways implicated in thrombus formation. Clinicians should recognize that individuals with iron deficiency and concomitant SARS-CoV-2 or influenza infection may be at increased risk of arterial and venous thrombosis, atrial fibrillation, and viral myocarditis. Given that approximately two billion people worldwide have some degree of iron deficiency—especially older adults and young children—appropriate preventive strategies should be considered.

Graphical Abstract