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Most people contract the herpes virus at an early age. After a single infection, the viruses remain in the body for life. The eight known human herpes viruses include the herpes simplex virus, responsible for the well-known vesicles in the mouth area, the chickenpox and shingles virus, responsible for chicken pox and shingles , and the Epstein-Barr virus, responsible for glandular fever. and is also involved in the development of many cancers. Although herpesvirus infections do not significantly affect the health of most people, patients whose immune systems are severely compromised, such as those who have been transplanted, have difficulty controlling the virus. This can lead to rejection reactions and serious organ damage or even death.
TRIM43 inhibits the proliferation of herpesviruses
To counter the risks badociated with herpes viruses, scientists at the Institute of Virology at the University Hospital Erlangen are looking for endogenous proteins that can contain viruses. "We are interested in the so-called intrinsic immune response, ie protein molecules that can prevent the multiplication of viruses directly into cells," says Dr. med. Full. The research team discovered the so-called TRIM proteins. TRIM stands for "tripartite motif", a three-part protein motif that binds and breaks down other proteins. It has been shown that one of the TRIM proteins, TRIM43, which was not previously described, causes the degradation of another cellular protein called pericentrin. The degradation of pericentrin causes 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 new therapies
Remarkably, the cells produce very large amounts of TRIM43 in response to the viral infection. "In normal cells, TRIM43 is almost undetectable, but after a viral infection, the cell is full of protein," says Dr. Plein. In collaboration with dr. Klaus Korn, Head of Viral Diagnosis at the Institute of Virology, and Prof. Dr. med. Michael Stürzl, Head of Molecular and Experimental Surgery at the Surgical Clinic (Director: Professor Robert Grützmann) of the Erlangen University Hospital, showed the research team that a increased TRIM43 protein in samples of patients with acute herpesvirus infection and even tumor cells carrying a herpes virus are detectable. "This proves that TRIM43 plays a role in the infection in humans and gives hope that it would be possible to develop new treatments for herpesvirus based on the results," concludes Florian Full.
In addition, the team of researchers has demonstrated that the production of TRIM43 in response to a viral infection is dependent on DUX4, a gene that, under normal circumstances, is active only very early in embryonic development. Why does herpesvirus infection lead to activation of the embryonic DUX4 gene, and what is a previously unknown immune response to viruses, is the subject of a new research project from the University of Erlangen, the Interdisciplinary Center for Clinical Research of the Medical Faculty Center of the Friedrich-Alexander University of Erlangen-Nuremberg as part of a sub-project of a duration of 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, United States and University of Chicago, Chicago, United States) and is at the Institute of Virology at Erlangen University Hospital in Prof. Lab. Dr. med. Armin Ensser continued.
scientific contact:
Dr. Florian Full
Phone: 09131 85-26494
[email protected]
Original publication:
www.dx.doi.org/10.1038/s41564-018-0285-5
idw 2018/11
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