Herpes viruses are among the viruses that remain in the body forever. However, a healthy immune system keeps the attackers under control. How this works, researchers have now discovered.
Herpes are not the same as herpes. 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. What they all have in common is that they stay in the body for life. Nearly every person has been infected with herpes virus in her childhood.
When herpes wake up
A healthy immune system can keep a herpes virus nearby. However, if the immune system is weakened for some reason, the herpes virus can repeat. Either visible in the mouth or genital area or like painful nails. In addition, a transplant can lead to rejection reactions threatening life and serious organ damage due to the recovery of herpesviruses.
To avoid these hazards, researchers are looking for the mechanisms that help keep herpes under control. The scientists of the Erlangen University Hospital of the University and the University of Chicago have now discovered what they are looking for. The work has been published in the current edition of the "Nature Microbiology" magazine.
New findings on the immune response
"We are interested in the indigenous immune response as it is called, ie protein molecules that can prevent virus multiplication directly in cells," explains Dr. Virologist. med. Florian Full of the University of Erlangen. In the investigations, researchers came across tripartic motif proteins, TRIM for a short period. There is a three-part protein motif that can bind other proteins and cause their degradation. The researchers were able to show that one of the TRIM proteins, the TRIM43 previously described, caused a degradation of other cellular protein of the pericentrinous name.
The TRIM43 protein could play a key role in new therapies
"The analysis of pericentrin results in changes in the kernel's architecture and thus obstructs the number of herpesviruses. TRIM43 was active against all the herpesviruses that were experienced in the study," explained Full .
It was particularly surprising that infected cells produced very large amounts of TRIM43. "In normal cells, TRIM43 is almost unstable, but after viral infection, the cell is full of protein," Dr Llawn. Even in tumor cells that carry herpesvirus, Trim 43 discovered. According to the virus researcher, this proves that TRIM43 plays a part in human herpes infections. Dr. Full: "We hope it's possible to develop new therapies for herpesviruses based on the results."
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