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New therapies: Herpes can be treated with the body's own protein


Antiviral mechanism: fight herpes with the body's own protein

According to health experts, two out of three people are infected with herpes viruses, the majority do not even notice it. But in some infected people, the highly contagious virus causes cold sores on the lips, among other things. And for some people, the pathogen can even be life-threatening. An international team of researchers has now determined that herpes is combated with an endogenous protein.

What helps against herpes

Herpes is extremely common. Once you are infected with the virus, you will never get rid of it. It slumbers to break out again and again in the form of annoying bubbles. Health experts usually advise infected people to treat cold sores as early as possible. But what helps against herpes? Among other things, an endogenous protein, as researchers have now found out.

Most people catch the virus in childhood

Most people acquire herpes viruses early in childhood. After a single infection, the viruses remain in the body for life.

The eight known human herpes viruses include the herpes simplex virus, which causes the known blisters in the mouth (herpes in the mouth), the varicella zoster virus, which causes chickenpox and shingles, and the Epstein-Barr virus, that triggers Pfeiffer's glandular fever and is also involved in the development of numerous cancers.

Although infections with herpes viruses do not have a lasting negative impact on health in most people, patients with a severely weakened immune system - for example after transplants - have difficulties in keeping the viruses under control.

This can lead to rejection reactions and severe organ damage and even death.

A herpes virus infection can also be fatal for babies, as various cases have shown.

In addition, the viruses are a possible trigger for mental illnesses.

The body defends itself against viruses

When we are infected by a virus, our body recognizes this attack and starts a whole cascade of defense reactions.

A research group led by Dr. Florian Full and Prof. Dr. Armin Ensser from the Virological Institute of the University Hospital Erlangen, in collaboration with researchers from the University of Chicago in the USA, has now discovered a new immune response against herpes viruses.

"Our results describe a previously unknown mechanism of the body's defense against herpes viruses," explains Dr. Full in a communication from the Friedrich Alexander University (FAU) Erlangen-Nuremberg.

The work was published in the current issue of the journal "Nature Microbiology".

The multiplication of the pathogens is inhibited

In order to counter the risks of herpes viruses, the researchers from Erlangen are looking for the body's own proteins that can keep the viruses at bay.

"We are interested in the so-called intrinsic immune response, that is, protein molecules that can prevent viruses from multiplying directly in the cells," explains Dr. Full.

The team of scientists found what they were looking for with so-called TRIM proteins. TRIM stands for “tripartite motif”, a three-part protein motif that can bind other proteins and cause them to break down.

The experts were able to show that one of the TRIM proteins, the previously unknown TRIM43, causes the degradation of another cellular protein called pericentrin.

The breakdown of pericentrin leads to changes in the architecture of the cell nucleus and thus inhibits the multiplication of the herpes viruses. TRIM43 was active against all herpes viruses tested in the study.

Hope for new therapies

It was remarkable that cells produce very large amounts of TRIM43 in response to the virus infection.

"TRIM43 is almost undetectable in normal cells, but after a virus infection the cell is full of the protein," says Dr. Full.

In collaboration with Dr. Klaus Korn, head of virus diagnostics at the Virological Institute, and Prof. Michael Stürzl, head of molecular and experimental surgery at the surgical clinic of the University Hospital Erlangen, were able to show that an increase in the TRIM43 protein also in patient samples with acute herpes virus infection and is even detectable in tumor cells that carry a herpes virus.

"This proves that TRIM43 plays a role in human infection and raises the hope that it could be possible to develop new therapies against herpes viruses based on the results," Full summarizes the results.

The team also demonstrated that TRIM43 production in response to a viral infection is dependent on DUX4 - a gene that, under normal circumstances, is only active in very early embryonic development.

Why the infection with herpes viruses leads to an activation of the embryonic gene DUX4, and whether this is a previously unknown immune response against viruses, is the subject of a new research project at the University Hospital Erlangen. (ad)

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Video: Antiherpes Virus Drugs Concepts for USMLENEETFMGEPLAB (January 2022).