Healing herpes with body proteins

Antiviral Mechanism: Fighting the body's own herpes protein

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

What helps against herpes

Herpes is extremely common. Once you get infected with the virus, it will not let you go. It sleeps to burst again and again in the form of annoying bubbles. Health experts usually advise infected people to treat cold sores as soon as possible. But what helps against herpes? Among other things, an endogenous protein, as the researchers have now discovered.

Most people catch the virus as early as childhood

Most people contract the herpes virus at an early age. After a single infection, the viruses remain in the body for life.

The eight known human herpes viruses include the herpes simplex virus, responsible for well-known oral vesicles (herpes in the mouth), chickenpox and shingles, responsible for chickenpox and chickenpox. shingles, and Epstein-Barr virus. which causes Pfeiffer's glandular fever and is also involved in the development of many cancers.

Although herpesvirus infections do not significantly affect the health of most people, patients whose immune systems are severely compromised, such as those who have been transplanted, have difficulty controlling the virus.

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

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

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

The body defends against viruses

When we are infected with 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 of the Institute of Virology at Erlangen University Hospital, in collaboration with researchers from the University of Chicago in the United States, has discovered a new defense response against herpes virus.

"Our results describe a mechanism until now unknown to the body to rule out herpes viruses," says Dr. Full in a message from the Friedrich Alexander University (FAU) Erlangen-Nuremberg.

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

The spread of pathogens is inhibited

To counter the risks badociated with herpesviruses, Erlangen researchers are looking for endogenous proteins capable of containing viruses.

"We are interested in the so-called intrinsic immune response, which is protein molecules that can prevent the proliferation of viruses directly into cells," said Dr. Plein.

The team of scientists discovered the so-called TRIM proteins. TRIM stands for "tripartite motif", a three-part protein motif that binds and breaks down other proteins.

Experts have been able to show that one of the TRIM proteins, the TRIM43, which had not yet been described, causes the degradation of another cellular protein called pericentrin.

The degradation of pericentrin causes 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 new therapies

Remarkably, the 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," says Dr. Plein.

In collaboration with dr. Klaus Korn, Head of Viral Diagnosis at the Institute of Virology, and Prof. Dr. med. Michael Stürzl, Head of Molecular and Experimental Surgery at the Surgical Clinic of Erlangen University Hospital, showed that an increase in TRIM43 protein was also detectable in samples of patients with an infection acute herpes and even in tumor cells carrying a herpes virus.

"This proves that TRIM43 plays a role in human infection and gives hope that it would be possible to develop new treatments for herpes-based herpes viruses," Full said.

In addition, the team has 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 very early in embryonic development.

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