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Lactoferrin as a prevention of COVID-19

The COVID-19 pandemic has created the need for multiple medical trials of medications to treat the latter.
Much of the medication that was considered effective at the beginning of the pandemic has now been rejected by medical science.
The features of spread and the symptoms displayed by patients with COVID-19 made it necessary to look for preparations that have a curative and prophylactic effect, based on an antiviral effect and an immunomodulatory effect.

A study by scientists from Thailand and China published in April 2020. shows encouraging data regarding the application of Lactoferrin which is also the active ingredient contained in branded products Biozin and Cavisept on prevention and initial treatment of COVID-19 infection.

The novel coronavirus (COVID-19) pandemic, which began in 2019, is rapidly spreading around the world despite drastic public and personal health measures being taken. Antivirals and nutritional supplements have been proposed as potentially useful agents against SARS-CoV-2 (the virus that causes COVID-19), but few have been clinically established as such.
Lactoferrin (Lf) is a naturally produced and non-toxic glycoprotein that is available for oral administration as a dietary supplement and has demonstrated in vitro antiviral efficacy against a wide range of viruses, including SARS-CoV, which is closely related to the SARS-CoV-2 coronavirus (the virus that causes COVID-19). In addition, Lf possesses unique immunomodulatory and anti-inflammatory effects that may be specifically related to the pathophysiology of severe cases of COVID-19. We address the underlying biological mechanisms of Lf as an antiviral and immune regulator and propose its unique potential as a preventive and adjunctive treatment in COVID-19.
We hope that further research and development of dietary supplements with Lf will determine its role in COVID-19.

LF for potential prevention and treatment of COVID-19
Lf has been shown to experimentally inhibit virus entry by attaching to HSPGs on the surface of host cells in coronavirus-infected mice (de Haan and authors, 2005), in human coronaviruses hCOV-NL63 (Milewska and authors, 2014) and in SARS-CoV pseudotype (Lang and authors, 2011). There are still unpublished studies on the effect of Lf on SARS- CoV-2 and its entry into host cells. Nevertheless, given the currently accepted "virus surfing" model for the role of HSPGs on the cell surface (Burckhardt and Greber, 2009), according to which entering virion particles "surf" from HSPG attachment sites with weak affinity to entry receptors with strong affinity in the form of invasion, together with the homology of the spike protein structures of SARS-CoV and SARS-CoV-2, as well as the fact that both viruses depend on the same ACE2 receptor to enter cells (Hoffmann and authors, 2020), we are confident in our assertion that a similar mechanism is at work, with HSPGs serving as anchor sites for SARS-CoV-2 that crowd the virus onto the cell surface and facilitate specific entry receptors such as ACE2. Therefore, it is likely that Lf can inhibit SARS-CoV-2 invasion at micromolar concentrations and in a dose-dependent manner, as is the case with SARS-CoV (Lang and authors, 2011).
Another important aspect of Lf bioactivity is associated with its immunomodulatory and anti-inflammatory properties. In viral infections in particular, it is the extent of the immune response and inflammation that contribute to the severity of the disease, and this is especially true for COVID-19.
Current attitudes suggest that mortality from COVID-19 is not simply due to viral infection, but results from cytokine storm syndrome in certain patients associated with hyperinflammation leading to acute respiratory distress and subsequent mortality (Mehta and authors, 2020). The cytokine profile in severe cases of COVID-19 is characterized by increases in levels of cytokines and acute phase reactants such as interleukin IL-6, tumor necrosis factor-α (TNFα) and ferritin. In this regard, Lf reduced levels of IL-6, TNFα (Zimecki and authors, 1998) and ferritin (Rosa and authors, 2017) in an experimental setting simulating sepsis. If the hypothesis that Lf can modulate immune system overreaction and inflammatory mechanisms in response to viral infection is correct, then Lf could be a candidate adjunctive treatment for the more severe cases of COVID-19.

Conclusion
Over the past 30 years, great progress has been made in elucidating the multiple functions of lactoferrin (Lf) as an antiviral agent as well as a unique anti-inflammatory and immunomodulatory molecule. We have presented the experimental as well as clinical rationale for its use in COVID-19, but further research is needed to confirm its virus-inhibiting property, as well as clinical studies to clarify its dosage and efficacy and thus to confirm the potential of Lf for the prevention of SAR-CoV-2 as well as for the treatment of COVID-19.

For more detailed information about the publication, see the following link: https://www.researchgate.net/profile/Raymond_Chang4/publication/340464937_Lactoferrin_as_potential_preventative_and_treatment_for_COVID-19/links/5e8ba8c2a6fdcca789fbdb46/Lactoferrin-as-potential-preventative-and-treatment-for-COVID-19.pdf

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