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. 2022 Apr 25;13:878201. doi: 10.3389/fimmu.2022.878201

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Copyright © 2022 Bartolomé, Rosa, Valenti, Lopera, Hernández-Gallego, Cantero, Orive and Carro

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential role of Lf in the relationship between AD brain pathology and COVID-19. Pathogenic events leading to neuronal damage may impair the host defense system which in turn reduce AMP production, including Lf, and influence the extent of SARS-CoV-2 infection in the brain. Additionally, potential antiviral mechanisms of Lf are shown: (1) by modulating SARS-CoV-2 induced inflamation, reducing pro-inflammatory cytokine levels, such as IL-6 and TNFα; (2) by occupying binding sites of SARS-CoV-2, as heparan sulfate proteoglycans (HSPGs) on the host cell surface, reducing viral surfing and subsequent viral entry; and (3) by inhibition of viral replication via induction of intracellular cell signals. AD, Alzheimer’s disease; Lf, lactoferrin; AMP, antimicrobial peptide; BBB, blood-brain barrier.