• Marvin Edeas, Jumana Saleh, and Carole Peyssonnaux.
• Université de Paris, INSERM U1016, Institut Cochin, CNRS UMR8104, Paris, France; Laboratory of Excellence GR-Ex, Paris, France. Electronic address: marvin.edeas@inserm.fr.
• Int. J. Infect. Dis. 2020 Aug 1; 97: 303-305.

AbstractThe coronavirus 2 (SARS-CoV-2) pandemic is viciously spreading through the continents with rapidly increasing mortality rates. Current management of COVID-19 is based on the premise that respiratory failure is the leading cause of mortality. However, mounting evidence links accelerated pathogenesis in gravely ill COVID-19 patients to a hyper-inflammatory state involving a cytokine storm. Several components of the heightened inflammatory state were addressed as therapeutic targets. Another key component of the heightened inflammatory state is hyper-ferritinemia which reportedly identifies patients with increased mortality risk. In spite of its strong association with mortality, it is not yet clear if hyper-ferritinemia in COVID-19 patients is merely a systemic marker of disease progression, or a key modulator in disease pathogenesis. Here we address implications of a possible role for hyper-ferritinemia, and altered iron homeostasis in COVID-19 pathogenesis, and potential therapeutic targets in this regard.Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.

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