Studies

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Lactoferrin for the prevention of common viral infections

H. Wakabayashi, HirotsuguOda, Koji Yamauchi, Fumiaki Abe Institute of Food Science and Technology, Morinaga Mil Industry Co. Ltd., Japan © 2014, Japan Chemotherapy Society and Japan Infectious Diseases Association.

Summary

Although lactoferrin has many biological functions, one of the most important among them is the protection of the host against pathogenic microorganisms including bacteria, fungi and viruses. In this article, we review a study of the protective role of prescribed lactoferrin treatment against common viral infections. Many studies have shown that the in vitro antiviral activity of lactoferrin against viral pathogens causing common infections such as colds, influenza, gastroenteritis, summer flu, and herpes involves inhibition of the virus's attachment to target cells. In recent years, the number of studies indicating the in vivo protective effect of lactoferrin prescribed for oral use against common viral infections has increased. For example, norovirus is a very important emerging human aptogen,which is the cause of most outbreaks of gastroenteritis in the world and could be a target candidate for lactoferrin administration. Lactoferrin reduction reduced the incidence of norovirus-induced gastroenteritis in children, and in a preliminary study, a similar effect was observed in patients of all ages. A recent in vitro study reported that lactoferrin inhibited both the cellular attachment of norovirus in mice, a virus that is closely related to human norovirus, and the replication of the virus in cells by inducing the antiviral cytokine interferon (IFN) -α / ß. The administration of lactoferrin also improves the activity of NK cells and the response of Th1 cytokines, which leads to protection against viral infections. In conclusion,Lactoferrin intake can protect the host from viral infections by inhibiting the attachment of the virus to the cells, the multiplication of the virus in the cells and the improvement of the functions of the immune system.

Source

J Infect Chemother 20 (2014) 666e671

Inhibition of SARS pseudovirus entry into cells by binding of lactoferrin to heparansulphate proteoglycans

Jianshe Lang, Ning Yang, Jiejie Deng, Kangtai Liu, Peng Yang, Guigen Zhang, Chengyu Jiang Basic State Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, United Medical College of Beijing, Tsinghua University, Beijing, People's Republic of China

Summary

Lactoferrin (LF) has been reported to be involved in the host's immune response against the invasion of severe acute respiratory coronavirus syndrome (SARS-CoV), improving the action of natural killer cells (NK cells) and stimulating neutrophil accumulation and adhesion. We also 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 analyzes suggest that LF is able to block the binding of the spiny protein to host cells at 4 ° C, which is an indication that LF is exercising its inhibitory function at the stage of virus attachment. However, LF does not impair the interaction of thorn protein with angiotensin-converting enzyme-2 (ACE2),the functional SARS-CoV receptor. Previous studies have shown that LF localizes heparan sulfate proteoglycans (HSPGs), which are widespread on the cell surface. Our experiments also confirmed this conclusion. Treatment of cells with heparinase or exogenous heparin prevented the binding of the spiny protein to host cells and inhibited SARS pseudovirus infection, demonstrating that HSPGs provide the binding site for SARS-CoV invasion in the early attachment phase. Taken together, our results suggest that, in addition to ACE2, HSPGs are extremely important cell surface molecules involved in the entry of SARS-CoV into cells.LF may play a protective role in protecting the host against SARS-CoV infection by binding to HSPG and blocking pre-interaction between SARS-CoV and host cells. Our findings may help to better understand the pathogenesis of SARS-CoV and to treat this deadly disease.

Source

PLoS ONE | www.plosone.org | August 2011 | Volume 6 | Issue 8 | e23710

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