Antiviral mechanism: fight with the body's own herpes protein
According to health experts, two out of three people are infected with the herpes virus, the majority don't even notice. But in some people infected, the cause of infection is very contagious, among others, cold sores on the lips. And for some people, pathogens can even become life threatening. An international research team has now found that herpes fights with body proteins.
What helps fight herpes
Herpes is very widespread. After you infect yourself with the virus, the virus will not disappear. This slips to come out again and again in the form of annoying bubbles. People who are infected are usually advised by health experts to treat cold sores as early as possible. But what helps fight herpes? Among other things, endogenous proteins, as found by researchers.
Most people catch viruses as early as childhood
Most people get the herpes virus as early as a baby. After one infection, the virus stays in the body for life.
The eight known human herpes viruses include the herpes simplex virus, which causes known mouth blisters (herpes in the mouth), the varicella-zoster virus, which causes smallpox and rashes, and the Epstein-Barr virus, which causes Pfeiffer's glandular fever and is also involved in development a number of cancers.
Although herpes virus infection does not significantly affect the health of most people, patients with very weak immune systems, such as after a transplant, have difficulty controlling the virus.
This can cause severe rejection and organ damage reactions, including death.
Even for babies, infection with the herpes virus can be fatal, as shown in several cases.
In addition, the virus is a possible trigger for mental illness.
The body defends itself against the virus
When we are infected with a virus, our body recognizes this attack and launches a total defense response.
The research group around Dr. Florian Complete and Prof. Dr. med. Armin Ensser from the Virology Institute of the Erlangen University Hospital, working with researchers from the University of Chicago in the United States, is now finding a new defense reaction to the herpes virus.
"Our results illustrate the hitherto unknown mechanism of the body to ward off the herpes virus," explained Dr. Full in messages from Friedrich Alexander University (FAU) Erlangen-Nuremberg.
This work has been published in the latest issue of the journal "Nature Microbiology".
Pathogen propagation is inhibited
To overcome the risk of the herpes virus, researchers from Erlangen looked for endogenous proteins that can keep the virus at bay.
"We are interested in what is called the intrinsic immune response, a protein molecule that can prevent the proliferation of viruses directly in cells," Dr. Full.
The team of scientists discovered what is called the TRIM protein. TRIM stands for "tripartite motif", a three-part protein motif that can bind to other proteins and cause degradation.
Experts were able to show that one of the TRIM proteins, TRIM43 which had not been previously described, caused degradation of another cellular protein called pericentrin.
Pericentrin damage causes changes in the nucleus architecture and thus inhibits the proliferation of the herpes virus. TRIM43 is active against all herpes viruses tested in this study.
Hope for new therapies
Remarkably, the cell produces a very large amount of TRIM43 in response to viral infections.
"In normal cells, TRIM43 is almost undetectable, but after a viral infection, the cell is full of protein," Dr. Full.
In collaboration with Dr. Klaus Korn, Head of Virus Diagnostics at the Virology Institute, and Prof. Dr. med. Michael Stürzl, Head of Molecular and Experimental Surgery at the Erlangen University Hospital Surgery Clinic, the research team showed that an increase in TRIM43 protein was also detected in samples of patients with acute herpesvirus infections and even in tumor cells carrying the herpes virus.
"This proves that TRIM43 plays a role in human infections and raises hopes that it is possible to develop new therapies for herpes virus based on results," Full said.
In addition, the team showed that the production of TRIM43 in response to DUX4-dependent viral infections, genes that were normally only active in early embryo development.
Why infection with the herpes virus leads to the activation of the DUX4 embryo gene, and whether it is generally an unknown immune response to the virus, is the subject of a new research project at Erlangen University Hospital. (Ad)