Abstract
Viruses invade cells to reproduce, and they require an iron-filled cell for efficient reproduction. Together with other viruses, the coronavirus disease-2019 (COVID-19) virus can alter the expression of proteins involved in iron homeostasis. For example, in COVID19 patients, an increase in pro-inflammatory cytokines such as interleukin-6 may stimulate the synthesis of hepcidin, the regulatory hormone of iron metabolism, thereby suppressing ferroportin-mediated cellular iron export. Increased serum levels of ferritin in COVID19 virus infection is associated with a poor prognosis and may be partly due to the virus itself. Some viruses selectively infect iron acceptor cells (e.g. macrophages) by binding to transferrin receptor 1during cell entry. Moreover, human airway secretions in the major route of entry of COVID-19 include transferrin and lactoferrin, and this glycoproteins can bind iron and maintain a chemically inert form. Understanding how iron metabolism and viral infection interact in the COVID-19 outbreak may suggest new ways to control the disease.
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