New therapies treat herpes with endogenous protein

New therapies treat herpes with endogenous protein / Health News

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

According to health experts, two out of three people are infected with herpesviruses, the majority does not even notice. But in some infected the highly infectious virus causes, among other things, cold sores on the lips. And for some people, the pathogen can even become life-threatening. An international research team has now found that herpes is fought with a body protein.


What helps against herpes

Herpes is extremely widespread. Anyone who has once been infected with the virus will not let go. It slumbers to break out again and again in the form of annoying bubbles. Infected people are usually advised by health experts 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.

The blisters that develop in the case of an infection with herpesviruses in the mouth area, can be quite annoying. Researchers have now discovered a new defense response against the viruses. (Image: Janina Dierks / fotolia.com)

Most people catch the virus as early as childhood

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

The eight known human herpesviruses include, among others, the herpes simplex virus, which causes the familiar mouth blisters (herpes in the mouth), the varicella-zoster virus, which causes chickenpox and shingles, and the Epstein-Barr virus, which causes the Pfeiffersche glandular fever and is also involved in the development of numerous cancers.

Although herpesvirus infections do not significantly affect health in most people, patients with severely compromised immune systems, such as those after transplantation, have difficulty controlling the virus.

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

Even for babies, a herpes virus infection can be fatal, as several cases have shown.

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

The body defends itself against viruses

When we get infected by a virus, our body recognizes this attack and launches a whole cascade of defense responses.

A research group around Dr. Florian Full and Prof. Dr. med. Armin Ensser from the Virology Institute of the University Hospital Erlangen, in collaboration with researchers from the University of Chicago in the USA, now discovered a new defense reaction against herpesviruses.

"Our results describe a hitherto unknown mechanism of the body to ward off herpesviruses," explains Dr. Full in a message from the Friedrich Alexander University (FAU) Erlangen-Nuremberg.

The work has been published in the current issue of the journal Nature Microbiology.

Propagation of the pathogens is inhibited

To counteract the risks of herpesviruses, the researchers from Erlangen are looking for endogenous proteins that can keep the viruses at bay.

"We're interested in the so-called intrinsic immune response, protein molecules that can prevent the proliferation of viruses directly in the cells," Dr. Full.

The team of scientists discovered so-called TRIM proteins. TRIM stands for "tripartite motif", a three-part protein motif that can bind other proteins and cause their degradation.

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

The breakdown of pericentrin leads to changes in the architecture of the nucleus and thus inhibits the proliferation of herpesviruses. TRIM43 was active against all herpesviruses tested in the study.

Hope for new therapies

Remarkably, cells produce very large amounts of TRIM43 in response to the viral infection.

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

In collaboration with dr. Klaus Korn, Head of Virus Diagnostics at the Virological Institute, and Prof. Dr. med. Michael Stürzl, Head of Molecular and Experimental Surgery at the Surgical Clinic of the University Hospital Erlangen, the research team showed that an increase in the TRIM43 protein in patients with acute herpesvirus infection and even in tumor cells that carry a herpes virus, is detectable.

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

In addition, the team demonstrated that the production of TRIM43 in response to a viral infection is dependent on DUX4, a gene that under normal circumstances is active only in very early embryonic development.

Why the infection with herpesvirus leads to an activation of the embryonic gene DUX4, and whether it is generally a hitherto unknown immune response against viruses, is the subject of a new research project at the University Hospital Erlangen. (Ad)