Monday , June 14 2021

Fighting herpes with the body's own protein

Antiviral mechanism: Fight with the herpes protein of the body itself

According to health experts, two out of three people infected with herpes viruses, the majority did not even notice. But in some infected virus infection greatly causes, among other things, cold sores on the lips. For some people, the pathogen can even become life-threatening. An international research team has now found that herpes is fighting with the body protein.

What helps against herpes

Herpes is very common. Once you have yourself infected with a virus, it will not let go. This slumbers break out again and again in the form of annoying bubbles. Infected people are usually recommended 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 discovered now.

Blisters develop an infection with herpes viruses in the mouth area, and can be quite annoying. Researchers have now discovered a new defense response against viruses. (Photo: Janina Dierks /

Most people catch the virus already in childhood

Most people purchase herpesviruses already in infancy. After a single infection, the viruses remain in the body for life.

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

Although herpes infections do not significantly affect health in most people, patients with severe 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, herpes virus infection can be fatal, as some cases have shown.

In addition, viruses are a possible cause of mental illness.

The body protects itself against viruses

When we are infected with the virus, our body recognizes this attack and triggers a whole cascade of security responses.

A research group around Dr. Florian Mela and Prof. Dr. Med. Armin Ansar of the Erlangen University Hospital's virological institute, in collaboration with researchers at the University of Chicago in the United States, has now discovered a new defense response against herpes.

"Our results describe an unknown mechanism so far of the body to ward off herpes," explains Dr. Mela in a statement from the University of Friedrich Alexander (Arlungen-Nuremberg).

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

The proliferation of pathogens is delayed

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

"We want the essential immune responses, protein molecules that can prevent the spread of viruses directly in cells." full.

The team of researchers discovered what are called TRIM proteins. TRIM represents a three-piece motif, a three-part protein motif that can tie other proteins to their degradation.

The experts have shown that one of TRIM43's untimely dries, the untested TRIM43, has the effect of other extracellular proteins called pericentrin.

Nutrin breakdown leads to changes in the architecture of the nucleus, thus inhibiting the spread of the herpesvirus. TRIM43 was active against all the rhesus viruses tested in the study.

Hope for new treatments

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

"In normal cells, TRIM43 is almost unrecognizable, but after a viral infection, the cell is filled with protein." full.

In collaboration with Dr. Klaus Koren, director of virus diagnostics at the Institute of Virology and Prof. Dr. Med. Michael Storzel, head of molecular and experimental surgery at the surgical clinic of Erlangen University Hospital, has shown that an increase in TRIM43 is also evident in samples of patients with acute acute inflammation, even in tumor cells carrying herpes virus.

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

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

Why does the infection with herpes lead to the activation of the fetal DUX4 gene, and whether it is usually an unknown immune response so far against viruses, is the subject of a new research project at Erlangen University Hospital. (ad)

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