FAU: Combat Herpes with the body's own protein



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Most people get herpes virus as early as childhood. After a single infection, viruses remain in the body for life. The eight known human herpesviruses include the herpes simplex virus, which causes familial blisters in the mouth region, the varicella-zoster virus that causes chickenpox and the zone, and the Epstein-Barr virus, which causes glandular fever. and is also involved in the development of many types of cancer. Although herpesvirus infections do not significantly affect health in most people, patients with severely compromised immune systems, such as those after transplantation, have difficulty controlling the virus. This can lead to rejection reactions and serious organ damage, including death.

TRIM43 inhibits herpesvirus proliferation
To combat the risks of herpes virus, scientists at the Virological Institute at Erlangen University Hospital are looking for endogenous proteins that can keep viruses under control. "We are interested in the so-called intrinsic immune response, protein molecules that can prevent the multiplication of viruses directly in cells," explains Dr. med. Complete. The research team discovered the so-called TRIM proteins. TRIM stands for "tripartite motif," a three-part protein motif that can bind other proteins and cause them to break down. It has been shown that one of the TRIM proteins, TRIM43 previously not described, causes the degradation of another cellular protein called pericentrin. The breakdown of pericentrine leads to changes in the nucleus architecture and therefore inhibits herpesvirus proliferation. TRIM43 was active against all herpesviruses tested in the study.

Hope for new therapies
Notably, cells produce very large amounts 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," Dr. Full says. In collaboration with dr. Klaus Korn, Head of Virus Diagnosis at the Virological Institute, and Prof. Dr. med. Michael Stürzl, Head of Molecular and Experimental Surgery at the Surgical Clinic (Director: Prof. Dr. Robert Grützmann) at the University Hospital of Erlangen, showed the research team that an increase in TRIM43 protein in samples from patients with acute herpesvirus infection and even in tumor cells carrying the herpes virus are detectable. "This proves that TRIM43 plays a role in human infection and raises the hope that it will be possible to develop new therapies for herpesvirus based on the results," concludes Florian Full.

In addition, researchers have shown that production of TRIM43 in response to a viral infection is dependent on DUX4, a gene that under normal circumstances is active only in early embryonic development. Because herpesvirus infection leads to an activation of the DUX4 embryonic gene, and if it is usually a previously unknown immune response against viruses, it is the subject of a new research project at the University of Erlangen, the Interdisciplinary Clinical Research Center of the Faculty of Medicine. Faculty of the Friedrich-Alexander Erlangen-Nürnberg University under a sub-project for two and a half years.

The scientific work was done by Dr. med. Florian Full in the laboratory of Prof. Dr. med. Michaela Gack (Harvard University, Boston, USA and University of Chicago, Chicago, USA) and is at the Virological Institute of the University Hospital of Erlangen in the laboratory of Prof. Dr. med. Armin Ensser continued.

scientific contact:
Dr. Florian Full
Tel: 09131 85-26494
[email protected]

Original Publication:
www.dx.doi.org/10.1038/s41564-018-0285-5

idw 2018/11

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