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.
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. "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. 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.
I look forward to new therapies
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.
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.
Dr. Florian Full
Phone: 09131 85-26494