A protein produced by the human immune system may strongly inhibit corona viruses, including Sars-Cov-2, the pathogen causing Covid-19. An international team from Germany, Switzerland and the USA successfully showed the LY6E-Protein prevents coronaviruses from causing the illness.

"This finding may result in the development of new therapeutic approaches against coronaviruses," says Professor Stephanie Pfänder from the Department for Molecular and Medical Virology at Ruhr-Universität Bochum (RUB), lead author of the study published by the team in the journal Nature Microbiology on 23 July 2020.

<strong>Strengthening flu viruses, impairing corona viruses</strong>
The LY6E protein plays a role in various diseases: US researchers Professor John Schoggins and Professor Charles Rice found that the protein enhances the infectivity of influenza viruses.

Founded by a Marie Curie Individual Fellowship of the European Union, Stephanie Pfänder, who was then working in the Institute of Virology and Immunology in Switzerland, visited Charles Rice's lab at Rockefeller University in New York in 2017, in order to identify genes that prevent coronavirus infections.

<span style="color: #ff6600;"><a style="color: #ff6600;" href="https://news.rub.de/english/press-releases/2020-07-28-virology-immunoprotein-impairs-sars-cov-2">"This led to the discovery which LY6E has the opposite effect on coronaviruses when compared with flu viruses," explains the researcher. Further investigations revealed that the protein exerted this inhibitory effect on all examined coronaviruses, such as the germs causing Sars and Mers and Sars-Cov-2 which causes Covid-19.</a></span>

Viruses not able to fuse
Tests with different cell cultures showed that LY6E affects the ability of the virus to fuse with the host cells.

<span style="color: #ff6600;"><a style="color: #ff6600;" href="https://news.rub.de/english/press-releases/2020-07-28-virology-immunoprotein-impairs-sars-cov-2">The validation in an animal model succeeded thanks to a collaboration with the lab of John Schoggins in the Southwestern Medical Center at the University of Texas.</a></span> The experiments conducted there resulted in the discovery that the mouse variant of this protein called Ly6e is vital for the protection of immune cells against infections.

In the absence of Ly6e, immune cells like dendritic cells and B-cells become more vulnerable to disease and their numbers decrease radically. Mice lacking Ly6e in immune cells are highly susceptible to some normally non-lethal mouse coronavirus and succumb to infection.

<strong>Knowing basic concepts</strong>
The researchers point out that the mouse coronavirus used in the experiment differs considerably in the pathogen causing the current Covid-19 outbreak - for example, it causes hepatitis rather than respiratory disease. Regardless, it's widely recognized as a model for understanding the basic theories of coronavirus replication and immune reactions in a living creature.

<span style="color: #ff6600;"><a style="color: #ff6600;" href="https://news.rub.de/english/press-releases/2020-07-28-virology-immunoprotein-impairs-sars-cov-2">"Our study offers new insights into just how significant these antiviral genes are for the control of viral infection and for a decent immune response against the virus," stated the authors.</a></span>

"Since LY6E is a naturally occurring human protein, we expect that this knowledge will aid the development of therapies that may one day be used to take care of coronavirus infections." A therapeutic strategy that mimics the mechanism of activity of LY6E may provide the initial line of defense against publication coronavirus infections.
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<span style="color: #ff6600;"><a style="color: #ff6600;" href="https://news.rub.de/english/press-releases/2020-07-28-virology-immunoprotein-impairs-sars-cov-2" target="_blank" rel="noopener noreferrer">Ruhr-Universitaet-Bochum</a></span>

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Pfaender, S., <em>et al</em>. (2020) LY6E impairs coronavirus fusion and confers immune control of viral disease. <em>Nature Microbiology. </em><span style="color: #ff6600;"><a style="color: #ff6600;" href="https://doi.org/10.1038/s41564-020-0769-y" target="_blank" rel="noopener noreferrer">doi.org/10.1038/s41564-020-0769-y.</a></span>

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