Most people get herpesviruses as early as babies. After one infection, the viruses remain in the body for life. The eight human herpesviruses known include the herpes simplex virus, which causes the familiar buzzards in the mouth area, the varicella-zoster virus, which causes screws and eagles, and the Epstein-Barr firms, which cause chlandular fever and is also about developing a lot of cancer. Although herpesvirus infections do not really affect health in most people, patients with severe immune systems, such as those after transplant, have difficulty managing the virus. This can lead to rejection reactions and serious damage to the organ, including death.
TRIM43 hinders the number of herpesviruses
In order to address the challenges of herpesviruses, scientists of the Erlangen University Hospital of Virus Institute are looking for endogenous proteins that can keep viruses on the bay. "We are interested in the incredible indigenous immune response, protein molecules that can prevent virus multiplication directly in cells," explained Dr. Med. Full. The research team known as TRIM proteins discovered. TRIM stands for a "tripart motif", a three-part protein motif that can bind other proteins and cause their degradation. One of the TRIM proteins, the TRIM43 previously described, has been shown to cause a degradation of another cellular protein of the pericentrinous name. The pericentrin analysis results in changes in the nucleus's architecture and thus obstructs the number of herpesviruses. TRIM43 was active against all the herpesviruses tested in the study.
Hope for new therapies
Incredibly, cells produce very large quantities of TRIM43 in response to viral infection. "In normal cells, TRIM43 is almost unstable, but after viral infection, the cell is full of protein," Dr Llawn. In association with Dr. Klaus Korn, Head of Virus Diagnostics at the Institute of Physiology, and Professor Dr med. Michael Stürzl, Head of Molecular and Experimental Surgery in the Surgical Clinic (Director: Professor Dr Robert Grützmann) of Erlangen University Hospital & Research, showed that there was an increase in the TRIM43 protein in samples of patients with acute and up-to-date herpesvirus infection old Tone cells who can carry herpes virus can be found. "This proves that TRIM43 plays a part in human infection and raises the hope that new therapies for herpesviruses based on the results may be possible," Florian Full comes to a collection of the study.
In addition, the researchers team showed that the production of TRIM43 in response to viral infection depends on DUX4, a gene that only under normal circumstances is only active in very early embryonic development. Why the infection with herpesviruses leads to the operation of the DUX4 embryonic gene, and if the whole is an unknown virus anti-virus immune response, the subject of a new research project at Erlangen University, the Interdisciplinary Research Center Clinical in the Medical Faculty of Erlangen-Nürnberg Friedrich-Alexander-University within the scope of a sub-project for two and a half years.
The scientific work was carried out by Dr. Med. Florian Full in the laboratory of Professor Dr med. Michaela Gack (University of Harvard, Boston, USA and University of Chicago, Chicago, USA) and is a Physiological Institute of the University Hospital of Erlangen at the laboratory of Professor Dr Med. Armin Ensser continued.
Dr. Florian Full
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