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Can Lactoferrin Fight Coronavirus (COVID-19)?

Written by Carlos Tello, PhD (Molecular Biology) | Last updated:
Puya Yazdi
Medically reviewed by
Puya Yazdi, MD | Written by Carlos Tello, PhD (Molecular Biology) | Last updated:

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Note that each number in parentheses [1, 2, 3, etc.] is a clickable link to peer-reviewed scientific studies. A plus sign next to the number “[1+, 2+, etc...]” means that the information is found within the full scientific study rather than the abstract.

This article is for informational purposes only. The current coronavirus outbreak is an ongoing event and certain details may change as new information comes to light. No effective or FDA-approved products are currently available for the treatment of the new coronavirus (also known as SARS-CoV-2 or 2019-nCoV), although research is still ongoing.

Lactoferrin is a glycoprotein produced by glands and white blood cells (neutrophils) during inflammation that has strong antibacterial, antiviral, and immunoregulatory activity [1].

Lactoferrin can exert changes on white blood cells, through increasing natural killer cell, neutrophils, and macrophage activities. This increases cytokine, and nitric oxide production as well as limits pathogen growth [2, 3, 4]. Lactoferrin also affects adaptive immune cells (T-cells and B-cells) [5].

Anti Infection Potential

Unfortunately, there have been no studies on lactoferrin and SARS-CoV-2 or COVID-19. While it does have some general anti-infection properties, it’s impossible to know if it can benefit COVID-19 in any way.

The following is some general anti-infection properties:

In 2 clinical trials on 312 bottle-fed babies, supplementation with bovine lactoferrin reduced the incidence of respiratory tract infections and symptoms such as running nose, cough, and wheezing [6, 7].

A combination of lactoferrin and whey protein reduced the incidence and severity of common colds in another trial on 126 people [8].

A study on 10 people infected with SARS-CoV-1 found that the infection increased lactoferrin production by 150x [9].

In cells, lactoferrin blocked molecules on the cell-surface commonly used by viruses as attachment sites (heparan sulfate proteoglycans), thus preventing a SARS-CoV-1 variant incapable of replicating (SARS pseudovirus) from invading them [10].

Lactoferrin is also active against other viruses. In a preliminary study of 11 patients with chronic hepatitis C (CHC), an 8‐week treatment of bovine lactoferrin (1.8 or 3.6 g/day) significantly reduced serum alanine transaminase (ALT) and the viral RNA in patients with milder forms of infection [11].

The same group of researchers then conducted a placebo-controlled trial of 63 CHC patients. They found that bovine lactoferrin (600 mg/day) produces a Th1-cytokine dominant environment (IL-4 and IFN-gamma), which supports the IFN therapy for hepatitis C [12].

Two additional studies of 310 CHC patients confirmed that lactoferrin may increase the effectiveness of standard treatment, but doesn’t have therapeutic properties on its own [13, 14].

In human cell cultures, lactoferrin can prevent viruses from entering human cells by blocking cellular receptors or directly binding to the viruses [15].

The bovine lactoferrin was more efficient than the human version in stopping the herpes virus in human cell culture. However, both types were able to stop the virus from entering the cells [16].

Lactoferrin was also effective in stopping the effects of HIV by blocking the entry process in vitro [17].

In human cells, lactoferrin also inhibited hepatitis B [18], HPV [19], rotavirus [20], respiratory syncytial virus [21], and influenza [22] by using similar mechanisms.

Lactoferrin helped reduce airway inflammation in a mouse asthma model [23]. Similarly, a lactoferrin spray reduced airway hyperreactivity and narrowing in asthmatic sheep [24]. In cells, it blocked histamine release [25]. 

In mice exposed to excessive oxygen levels (hyperoxia), a lactoferrin spray reduced lung injury and tissue scarring [26].

However, lactoferrin had no effect on virus replication or disease severity in mice infected with respiratory syncytial virus [27].

About the Author

Carlos Tello

Carlos Tello

PhD (Molecular Biology)
Carlos received his PhD and MS from the Universidad de Sevilla.
Carlos spent 9 years in the laboratory investigating mineral transport in plants. He then started working as a freelancer, mainly in science writing, editing, and consulting. Carlos is passionate about learning the mechanisms behind biological processes and communicating science to both academic and non-academic audiences. He strongly believes that scientific literacy is crucial to maintain a healthy lifestyle and avoid falling for scams.

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