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Lactoferrin (LF) is classically found in mammalian milk. It binds iron and has important immunological properties. One of the most well-known characteristics of LF is that it is antibacterial, antiviral, antifungal, anti-inflammatory, and anti-carcinogenic. Of particular interest, there is evidence that it can bind to at least some of the receptors used by coronaviruses and thereby block their entry.

Heparan Sulfate Proteoglycans (HSPGs) and the host receptor angiotensin-converting enzyme 2 (ACE2), as based on other activities lactoferrin might prevent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) from attaching to the host cells. Lactoferrin may consequently be of preventive and therapeutic value during the present COVID-19 pandemic.

LF is found in high quantities in human breast milk (specifically colostrum), as well as cow's milk. It is also an important component of the Mediterranean diet (which I strongly promote). Unlike milk, yogurt (or Kefir) has been through a fermentation process that includes an iron-binding protein called lactoferrin which helps to build strong bones. Lactoferrin increases the absorption of iron, which along with calcium, increases bone density. Kefir is a product made by kefir grains that degrade milk proteins into various peptides with health-promoting effects, including antithrombotic, antimicrobial and calcium-absorption enhancing bioactivities.

Neutrophils and Lactoferrin

LF plays an important role in host defense. LF also enhances natural killer cell activity in immune defense and can restrict the entry of the virus into host cells during infection. As part of the host's inflammatory response, leukocytes, including neutrophils, release LF from their granules, where it is normally stored. Activated neutrophils also release chromatin fibers, known as neutrophil extracellular traps (NETs), which trap and kill, amongst others, bacteria. These NETs likewise modulate both acute and chronic inflammation. NETs are also found in various autoimmune conditions such as rheumatoid arthritis, systemic lupus erythematosus.

Viruses and Lactoferrin

LF has strong antiviral activity against a broad spectrum of both naked and enveloped DNA and RNA viruses. LF inhibits the entry of viral particles into host cells, either by direct attachment to the viral particles or by blocking their cellular receptors. Some of the viruses that LF prevents from entering host cells e.g., Herpes simplex virus, human papillomavirus, human immunodeficiency virus (HIV), and rotavirus. These viruses typically utilize common molecules on the cell membrane to facilitate their invasion into cells, including HSPGs. HSPGs provide the first anchoring sites on the host cell surface, and help the virus make primary contact with these cells. HSPGs can be either membrane bound, or in secretory vesicles and in the extracellular matrix. It has been shown that LF is able to prevent the internalization of some viruses by binding to HSPGs.

COVID-19 and Lactoferrin

COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Many COVID-19 patients develop acute respiratory distress syndrome (ARDS), which leads to pulmonary edema and lung failure, and have liver, heart, and kidney damages. These symptoms are associated with a cytokine storm manifesting elevated serum levels of interleukin (IL) IL-1β, IL-2, IL-7, IL-8, IL-9, IL-10, IL-17, granulocyte colony-stimulating factor (G-CSF), Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF), interferon (IFN)γ, tumor necrosis factor (TNF)α, Interferon gamma-induced protein 10 (IP10), Monocyte Chemoattractant Protein-1 (MCP1), macrophage inflammatory protein 1(MIP1)A and MIP1B. IL-22, in collaboration with IL-17 and TNFα, induces antimicrobial peptides in the mucosal organs. IL-22 also upregulates mucins, fibrinogen, anti-apoptotic proteins, serum amyloid A, and LPS binding protein; therefore, IL-22 may contribute to the formation of life-threatening edema with mucins and fibrin, seen in SARS-CoV-22 and SARS-CoV patients.

The 2003 SARS-CoV strain, that also causes severe acute respiratory syndrome, attaches to host cells via host receptor ACE2. This type I integral membrane protein receptor is a well-known receptor for respiratory viruses, and is abundantly expressed in tissues lining the respiratory tract. During COVID-19 infection, SARS-CoV-2 also enters host cells via the ACE2 receptor. ACE2 is highly expressed on human lung alveolar epithelial cells, enterocytes of the small intestine, and the brush border of the proximal tubular cells of the kidney. HSPGs are also one of the preliminary docking sites on the host cell surface and play an important role in the process of SARS-CoV cell entry. There is no current confirmed information that SARS-CoV-2 binds to HSPGs, however, LF blocks the infection of SARS-CoV by binding to HSPGs. It is not presently known whether LF binds to ACE2, but it does bind to HSPGs.

Whether SARS-CoV-2 also enters host cells via HPSGs in the same way, as does (the 2003) SARS-CoV clearly warrants further investigation. Of particular interest, is the set of interactions between SARS-CoV-2 and host platelets. This is of importance, as COVID-19 infection, can cause hyperinflammation due to a cytokine storm. Pathogens like the influenza virus, do trigger life-threatening cytokine storms. Such a cytokine storm will significantly affect platelets, as platelets have many receptors where these inflammatory molecules may bind. Circulating cytokines and inflammatory markers will hyperactivate platelets, causing low platelet count (thrombocytopenia), and a significant chance of hypercoagulation. Thrombocytopenia is associated with increased risk of severe disease and mortality in patients with COVID-19, and thus serves as clinical indicator of worsening illness during hospitalization. Patients with type 2 diabetes are also particularly prone to increased levels of circulating inflammatory cytokines and hypercoagulation. COVID-19 patients without other comorbidities but with diabetes are at higher risk of severe pneumonia, excessive uncontrolled inflammatory responses and a hypercoagulable state. Guo and co-workers in 2020 also found that serum levels of IL-6, C-reactive protein, serum ferritin, and D-dimer, were significantly higher in diabetic patients compared with those without, suggesting that patients with diabetes are more susceptible to an inflammatory storm eventually leading to rapid deterioration of the patient with COVID-19.

In COVID-19 infection, LF may have a role to play in not only sequestering iron and inflammatory molecules that are severely increased during the cytokine burst, but also possibly in assisting in occupying receptors and HSPGs to prevent virus binding. Receptor occupancy is an important characteristic of LF, when taken as supplement. Furthermore, it may assist in preventing thrombocytopenia, and hypercoagulation, both prominent features of COVID-19 infection.

It is my recommendation to supplement your diet with fermented dairy products like Greek yogurt and Kefir to improve your overall health and wellness goals.

Kell et al. The Biology of Lactoferrin, an Iron-Binding Protein That Can Help Defend Against Viruses and Bacteria.



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