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. 2022 Jul 27;14(15):3090. doi: 10.3390/nu14153090

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Lactoferrin and viral infection. (A) Lactoferrin (Lf) can directly prevent viral entry through preventing viral engagement with host cell target receptors, such as hepatitis B virus (HBV) binding to glycosaminoglycan (GAG), hepatitis c virus (HCV) binding to cluster of differentiation 81 (CD81), and herpes simplex virus type 1 (HSV-1) binding to low-density lipoprotein receptor-related protein 1 (LRP1). (B) Lf uptake through the transferrin receptor (TfR) by host cells promotes the expression of antiviral genes and the inhibition of proinflammatory genes. (C) The proposed Lf mechanism in SARS-CoV-2 infection includes blocking viral binding to accessory target molecules, such as heparan sulfate proteoglycan (HS-PG) and sialic acid glycoprotein (SIA-PG), (D) direct binding to viral particles, and (E) the competitive inhibition of viral binding to the angiotensin-converting enzyme (ACE2) receptor. Additional abbreviations include: TGFB = transforming growth factor beta; IRF = interferon regulatory transcription factor; IFN = interferon; TLR = toll-like receptor; ICAM = intracellular adhesion molecule; IL = interleukin; TSLP = thymic stromal lymphopoietin.