Herpes viruses – almost none of them escape. Researchers nowadays believe that every adult has at least one of the best known people specializing in human herpes viruses. After infection, the herpes virus remains in the body's life. If it is weakened, in herpes simplex virus infection, blisters in the oral cavity have one of the harmful effects. Researchers have now identified a new antiviral mechanism against herpes viruses, which they believe will offer great potential for new therapeutic approaches.
Erlangen – Most people get herpes viruses early in their childhood. After one infection, the viruses remain in the body for life. Eight known human herpesviruses include the herpes simplex virus that causes known blisters in the mouth, the varicella-zoster virus that causes chickenpox and shingles and the Epstein-Barr virus that causes glandular fever and is also involved in the development of many cancers.
Although most people with herpesvirus infection do not significantly affect their health, patients with a seriously compromised immune system, such as those who after transplantation, have difficulty controlling the virus. This can lead to rejection reactions and severe damage to organs, including death.
In addition to the topic
Human herpes viruses and diseases caused by it
When we infect the virus, our body recognizes this attack and launches a comprehensive cascade of defense reactions. Research group at Dr. Florian Full and Prof. Dr. med Virgin Institute Armin Ensser (director Dr. Klaus Uberla) of the University of Erlangen, Germany, in collaboration with the US researchers at the University of Chicago, discovered a new defense response against herpes viruses.
TRIM43 inhibits the spread of herpesvirus
Researchers at the Erlangen University Hospital Virological Institute are looking for endogenous proteins that can keep viruses in the bay to prevent herpesvirus risks. When we infect the virus, our body recognizes this attack and launches a comprehensive cascade of defense reactions. Research Group at Dr. Florian Full and Prof. Dr. med Arlins Ensser of the Institute of Virusology (directed by Dr. Klaus Überla) University Hospital Erlangen has now discovered a new protective response to herpes viruses in collaboration with researchers from the University of Chicago in the United States.
"We are interested in the so-called natural immune response in protein molecules that can prevent the proliferation of viruses directly in the cells," explains Dr. med Full A team of researchers has discovered the so-called TRIM proteins. TRIM stands for "triangular motif", a three-part protein motif that can bind other proteins and cause them to degrade. "Our results describe the mechanism of an unknown body mechanism to prevent herpesviruses," says dr. Full
It has been shown that one of the TRIM proteins that was previously not described in TRIM43 causes the degradation of another fiber protein, called pericentryne. The degradation of percentrine leads to changes in kernel architecture and thus prevents the spread of herpesvirus. TRIM43 was active against all herpes viruses tested in the study.
Hope for new therapies against herpes viruses
Significantly, cells produce a very high amount of TRIM43 in response to a viral infection. "In normal cells, TRIM43 is almost undetectable, but after the virus infection, the cell is full of protein," Dr. Full In cooperation with Dr. Klaus Korn Virological Institute Virus Diagnostic Manager and Prof. Dr. med Michael Stürzl, head of the Department of Molecular and Experimental Surgery at the Surgical Clinic of the University Hospital of Erlangen (directed by Prof. Dr. Robert Grützmann) showed to the team of researchers that the increase in TRIM43 protein in patient samples with acute herpesvirus infection and even Flammable cells containing herpes virus can be detected . "It proves that TRIM43 is a human infection and it creates the hope that it will be possible to develop new therapies against herpes viruses based on the results," Florian Fully began studying.
The infection with herpes virus activates the embryonic gene
In addition, a team of researchers has shown that the production of TRIM43 in response to a viral infection depends on DUX4, a gene that, under normal conditions, operates only in the very early development of the embryo. Why is herpesvirus infection triggered by the activation of the embryonic DUX4 gene and is not usually the unknown immune response to viruses so far unknown, a new research project has been launched at the University of Erlangen at the Interdisciplinary Center for Clinical Trials at the Friedrich-Alexander-University University of Erlangen-Nirnberg Faculty for two and a half years.
The scientific work was done by Dr. med Florians Full Prof. Dr. med In the laboratory Michaela Gack (Harvard University, Boston, USA and Chicago University, Chicago, USA) and Prof. Dr. med Laboratory at the University Hospital in the Erlangen Virological Institute. Armin Ensser continued.
Original Publication: Florian Full, Michiel Van Gent, Constantine MJ Sparrer, Cindy Chiang, Matthew A. Zurensky, Myriam Scherer, Norbert H. Brockmeyer, Lucie Heinzerling, Michael Stürzl, Klaus Korn, Thomas Stamminger, Armin Ensser and Michaela U. Gack: Centrosome Protein TRIM43 restricts herpesvirus infection by regulating the integrity of nuclear material laminates; Natural Microbiology (2018)
Dr. S. Langer: University of Friedrich Alexander Erlangen-Nürnberg, 91054 Erlangen