Lactoferrin–An Antiviral and Immunogen

Do you like Milk? How about Cheese? Mayo? Ok, maybe I am reaching on that last one.

But all of these food sources have something in common. That’s a molecule known as Lactoferrin.

Say what?

Lactoferrin is a molecule that is involved in Iron transport within our bodies but more importantly, it is a potent antiviral against many forms of viruses including coronaviruses.

While you can get Lactoferrin from food sources, the quantity you will require is far too little unless you are downing gallons of milk or eating a block of cheese. I recommend 250 mg of Lactoferrin per day, which is taking 1 capsule per day of my recommended Lactoferrin in the Shop section.

Here’s the abstract of Lactoferrin in the context of Sars. Just a point of clarification. What you think of as the Wuhan, China Covid-19 virus is technically called Sars-Cov2 to us virologists. Sars-Cov1 would be the “original” Sars from 2003.

PLoS ONE 6(8): e23710
Inhibition of SARS Pseudovirus Cell Entry by Lactoferrin Binding to Heparan Sulfate Proteoglycans
Jianshe Lang, Ning Yang, Jiejie Deng, Kangtai Liu, Peng Yang, Guigen Zhang, Chengyu Jiang*

It has been reported that lactoferrin (LF) participates in the host immune response against Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) invasion by enhancing NK cell activity and stimulating neutrophil aggregation andadhesion. We further investigated the role of LF in the entry of SARS pseudovirus into HEK293E/ACE2-Myc cells. Our results reveal that LF inhibits SARS pseudovirus infection in a dose-dependent manner. Further analysis suggested that LF was ableto block the binding of spike protein to host cells at 4uC, indicating that LF exerted its inhibitory function at the viral attachment stage. However, LF did not disrupt the interaction of spike protein with angiotensin-converting enzyme 2 (ACE2), the functional receptor of SARS-CoV. Previous studies have shown that LF colocalizes with the widely distributed cell-surface heparan sulfate proteoglycans (HSPGs). Our experiments have also confirmed this conclusion. Treatment of the cells with heparinase or exogenous heparin prevented binding of spike protein to host cells and inhibited SARS pseudovirus infection, demonstrating that HSPGs provide the binding sites for SARS-CoV invasion at the early attachment phase. Taken together, our results suggest that, in addition to ACE2, HSPGs are essential cell-surface molecules involved in SARS-CoV cell entry. LF may play a protective role in host defense against SARS-CoV infection through binding to HSPGs and blocking the preliminary interaction between SARS-CoV and host cells. Our findings may provide further understanding of SARS-CoV pathogenesis and aid in treatment of this deadly disease.

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