Thursday , May 19 2022

Herpes that can be treated with endogenous protein



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Antiviral mechanism: the body's own protein herpesla combat

According to health professionals, two out of three people are infected with herpesvirus and the majority does not matter. But in some infected viruses, cold sores on the lips occur, among other things. And for some people, the pathogen can threaten life. An international research team has found that herpes fights with a body protein.

What helps against Herpes

Herpes is extremely common. Once you've infected yourself with the virus, it won't. In the form of annoying bubbles sweating repeatedly to crumple. Infected people are usually advised by health professionals to treat cold wounds as early as possible. But what helps against herpes? Among other things, as researchers have learned, an endogenous protein.

The bubbles that are infected with herpes viruses in the mouth may be quite annoying. Researchers have now discovered a new defense response to viruses. (Image: Janina Dierks / fotolia.com)

Most people catch the virus as early as childhood.

Most people get herpesvirus as early as infancy. After a single infection, viruses remain in the body for life.

Eight known human herpesviruses include the herpes simplex virus, which causes known oral blisters (herpes in the mouth), varicella zoster virus causing varicella and zona, and the Epstein-Barr virus. This leads to glandular fever of Pfeiffer and also plays a role in the development of numerous cancers.

Although herpesvirus infections do not significantly affect health in most people, patients with a severe immune system, such as post-transplantation, have difficulty in controlling the virus.

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

Even for babies, as shown in many cases, a herpes virus infection can be fatal.

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

Body protects itself against viruses

When infected by a virus, our body recognizes this attack and initiates a series of defense responses.

A research group around Dr. Dr. Florian Tam and Professor Dr. med. Armin Ensser from the Erlangen Virology Institute of the University Hospital, in collaboration with researchers from the University of Chicago in the US, discovered a new defense reaction to herpesviruses.

"Our results explain the body's unknown mechanism to stop herpesviruses," says Dr. The University of Friedrich Alexander (FAU) is filled with a message from Erlangen-Nuremberg.

The study was published in the current issue of "Nature Microbiology" magazine.

Propagation of pathogens is inhibited

To eliminate the risks of herpesviruses, researchers from Erlangen are looking for endogenous proteins that can hold viruses in the bay.

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

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

Experts could demonstrate that one of the TRIM proteins, TRIM43, which was not previously described, led to the degradation of another cellular protein called perisentrin.

Perisentrine deterioration 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 a very large amount of TRIM43 in response to viral infection.

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

Dr. Klaus Korn, Virus Diagnosis Manager and Professor at the Virology Institute. Dr. med. Michael Stürzl, chairman of the Department of Molecular and Experimental Surgery at the Erlangen University Hospital Surgery Clinic, showed that the increase in TRIM43 protein can be detected in patients with acute herpesvirus infection and even in tumor cells carrying a herpes virus.

Or This proves that TRIM43 plays a role in human infection and gives us hope that it is possible to develop new treatments for herpesviruses, “he says.

In addition, the team showed that the production of TRIM43 in response to a viral infection was due to DUX4 & apos; & quot; which is a gene that is active only under very early embryonic development under normal conditions.

Whether the herpesvirus infection leads to the activation of the embryonic gene DUX4, and whether there is so far an unknown immune response to the viruses, is the subject of a new research project at the University Hospital Erlangen. (Name)

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