Tuesday , July 27 2021

Fight against herpes with its own proteins

Antivirus Mechanism: Fight with Your Own Protein Herpes

According to health specialists, two out of three people are infected with herpes viruses, most noticed by them. However, in some infected highly infectious viruses, among others, cold sores on the lips. And for some people, a pathogen can even become life-threatening. The international research team has now found that herpes has fought with body protein.

What aids against herpes

Herpes is extremely widespread. After you get infected with the virus, you will not let go. Serve again and again in the form of boring bubbles. Infected persons usually advise health professionals to treat cold sores as early as possible. But what helps herpes? Among other things, endogenous protein, as the researchers have now discovered.

Bubbles that develop in the infection of herpes virus in your mouth may be very annoying. Researchers have now discovered a new defense response against the virus. (Photo: Janina Dierks / fotolia.com)

Most people catch the virus even in childhood

Most people are getting herpesviruses already in their childhood. After one infection, the viruses remain in the body for life.

Eight known human herpesviruses include herpes simplex virus, which causes known cavity cavities (mouthworms), varicella-zoster virus that causes swelling and shingles, and Epstein-Barr virus, causing Pfeiffer's glandular fever and is also involved in the development of numerous cancers .

Although infections of herpesviruses do not significantly affect the health of most people, patients with heavily endangered immune systems, such as those after transplantation, have difficulty in controlling the virus.

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

Even for babies, herpes virus infection can be deadly, as has been shown in several cases.

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

The body is protected from the virus

When we are infected with a virus, our body recognizes this assault and triggers the entire response cascade of defense.

Research group about Dr. Florian Full and Prof. Dr. Honey. Armin Ensser from the Virology Institute of the University Hospital Erlangen, in collaboration with researchers from the University of Chicago in the US, has now discovered a new response to herpes virus defense.

"Our findings describe an unknown body mechanism so far to prevent herpesviruses," explains Dr. Sc. Full in a message from Erlangen-Nürnberg University of Friedrich Alexander (FAU).

The paper was published in the current edition of the journal Nature Microbiology.

Propagation of the pathogen is inhibited

To counteract the risk of herpes virus, researchers from Erlangen seek endogenous proteins that can keep viruses.

"We are interested in the so-called Intrinsic Immune Response, Protein Molecules that can prevent virus proliferation directly in the cells," Dr. Full.

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

Experts may have shown that one of TRIM proteins, previously unreported TRIM43, causes degradation of another cellular protein called pericentrine.

Dissolution of pericentrine leads to changes in the core architecture and thus inhibits the proliferation of the herpes virus. TRIM43 was active against all herpesvirus tested in the study.

Hope for new therapies

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

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

In collaboration with Dr. Klaus Korn, Virus Diagnostic Manager at the Virology Institute and Prof. Dr. Honey. Michael Stürzl, the head of molecular and experimental surgery at the Erlangen University Hospital, said that the increase in TRIM43 protein can also be detected in samples of patients with acute infection of the herpes virus and even the herpes virus carrying tumor cells.

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

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

Why is infection with herpesvirus leading to the activation of the embryonic DUX4 gene and whether there is generally an unknown immune response to the virus, the subject of the new research project of the Erlangen University Hospital. (AD)

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