Monday , June 14 2021

Herpes with endogenous curable protein



Antivirus mechanism: fight against the body's cold sores

According to Health experts, two out of three people are infected with herpesviruses, and most do not even notice them. But in some infected with highly contagious virus causes, among others, herpes on the lips. For some people, the pathogen may even be life-threatening. An international research team has discovered that herpes is fought with body protein.

What helps with herpes

Herpes is extremely widespread. When you become infected with the virus, it does not let you go. It's napping to break out again in the form of annoying bubbles. Infected persons are usually advised by health experts to treat herpes as early as possible. But what helps in the fight against herpes? Among other things, an endogenous protein, as researchers have discovered.

Blisters that develop in the mouth sore virus infection can be quite annoying. Researchers have now found a new defense response against viruses. (Photo: Janina Dierks / fotolia.com)

Most people catch the virus as early as childhood

Most people acquire herpesviruses as early as childhood. After a single infection, the viruses remain in the body for the rest of their lives.

Eight known human herpesviruses include the herpes simplex virus, which causes known oral blisters (herpes in the mouth), varicella zoster virus that causes chicken pox and shingles, and Epstein-Barr virus, which causes Pfeiffer infectious mononucleosis, and also takes participation in the development of many cancers.

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

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

Even in infants, herpes infection can be fatal, as several cases have shown.

In addition, viruses can cause mental illness.

The body defends itself against viruses

When we are infected with the virus, our body recognizes this attack and launches a whole cascade of defensive reactions.

Research group around Dr. Florian Full and prof. Dr. Armin Ensser from the Virology Institute of the University Hospital of Erlangen, in collaboration with scientists from the University of Chicago in the USA, has now discovered a new defensive response to herpesviruses.

"Our results describe the previously unknown mechanism of the organism that protects herpesviruses" – explained Dr. A full message from the University of Friedrich Alexander (FAU) Erlangen-Nuremberg.

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

Propagation of pathogens is inhibited

To counteract the herpes-related risks, Erlangen researchers are looking for endogenous proteins that can stop viruses from being attacked.

"We are interested in the so-called Inner immune response, protein molecules that can prevent the proliferation of viruses directly in the" Full "cells.

A team of scientists has discovered so-called TRIM proteins. TRIM stands for a "tripartite theme", a three-part protein motif that can bind other proteins and cause them to degrade.

Experts have been able to show that one of the TRIM proteins, previously unspecified TRIM43, causes the degradation of another cellular protein called pericentrin.

Disintegration of pericentrin leads to changes in the architecture of the testis, and thus inhibits the proliferation of herpes viruses. TRIM43 was active against all herpes viruses tested in the study.

Hope for new therapies

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

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

In cooperation with dr. Klaus Korn, Head of Viral Diagnostics at the Virological Institute and prof. Dr. med. Michael Stürzl, Head of Molecular and Experimental Surgery at the Erlangen University Hospital Surgical Clinic, the research team showed that the increase in TRIM43 protein is also detectable in samples of patients with acute herpesvirus infection and even in cancer cells that carry herpes virus.

"This proves that TRIM43 plays a role in human infection and raises the hope that it will be possible to develop new herpesvirus therapies based on results," says Full.

In addition, the team showed that the production of TRIM43 in response to a viral infection depends on DUX4, a gene that under normal conditions is active only at a very early stage of embryonic development.

Why does herpes virus infection lead to the activation of the embryonic DUX4 gene and whether it is a generally unknown immune response to viruses, is the subject of a new research project at the University Hospital Erlangen. (Ad)


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