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Antian mechanism: struggle with herpes protein of the body
According to health experts, two out of three people are infected with herpes viruses, the majority does not even notice. But in some infected people, the highly contagious virus causes, among other things, cold sores on the lips. And for some people, the pathogen can even become life-threatening. An international research team has found that herpes is fought with body proteins.
What helps with herpes
Herpes is extremely widespread. Once you get infected with the virus, it will not let go. It wakes up to break out again and again in the form of annoying bubbles. Infected people usually consult with health experts to deal with cold sores as early as possible. But what helps against herpes? Among other things, an endogenous protein, as researchers now know.
Most people catch the virus ever since childhood
Most people get herpes viruses from their childhood. After a single infection, the viruses remain in the body for life.
The eight known human herpes viruses include herpes simplex virus, which causes the known oral blisters (herpes in the mouth), varicella-zoster virus causing varicella and herpes zoster and the Epstein-Barr virus, which causes glandular fever of Pfeiffer and also participates in the development of numerous cancers.
Although herpesvirus infections do not significantly affect the health of most people, patients with a severe immune system such as those following transplantation have difficulty controlling the virus.
This can lead to rejection reactions and serious organ damage, including death.
Even for babies, a herpesvirus infection can be lethal, as several cases have shown.
In addition, viruses are a potential cause of mental illness.
The body defends itself against viruses
When we infect a virus, our body recognizes this attack and starts a whole series of defense responses.
A research team around Dr. Florian Full and Professor Dr med. Armin Ensser of the Erlangen University Hospital, in collaboration with researchers at the University of Chicago in the US, has now discovered a new defense against the herpes virus.
"Our results describe an unidentified mechanism of the body to ward off herpes viruses," Dr. Full in a message from Friedrich Alexander University (FAU) Erlangen-Nuremberg.
The work was published in the current issue of Nature Microbiology.
Reproduction of pathogens is inhibited
To eradicate the dangers of herpes viruses, Erlangen researchers are looking for endogenous proteins that can keep viruses at bay.
"We are interested in the so-called inherent immune response, protein molecules that can prevent the proliferation of viruses directly into the cells.
The team of scientists discovered the so-called TRIM proteins. TRIM means "trimeric pattern," a three-dimensional protein pattern that can block other proteins and cause their degradation.
Those skilled in the art have been able to show that one of the TRIM proteins, the previously described TRIM43, does not cause degradation of another cellular protein called pericender.
The breakdown of pericardine leads to changes in the core architecture and therefore inhibits the proliferation of herpes viruses. TRIM43 was active against all herpes virus tested in the study.
Hope for new treatments
It is remarkable that cells produce very large amounts of TRIM43 in response to viral infection.
"In normal cells, TRIM43 is virtually undetectable, but after a viral infection, the cell is full of proteins," Dr. Complete.
In collaboration with Dr. Klaus Korn, Director of the Diagnostic Virus at the Institute of Virology, and Professor Dr. honey. Michael Stürzl, head of Molecular and Experimental Surgery at the Surgical Clinic at Erlangen University Hospital, showed that the increase in TRIM43 protein is also detectable in samples of patients with acute herpes infection and even herpesviruses bearing cancer cells.
"This demonstrates that TRIM43 plays a role in human infection and raises the hope that it could be possible to develop new treatments for herpesviruses based on results," says Full.
In addition, the group showed that the production of TRIM43 in response to a viral infection is dependent on DUX4, a gene that normally acts only in very early embryonic development.
Because herpes virus infection leads to activation of the embryonic gene DUX4 and if it is generally an unknown immune response to viruses, it is the subject of a new research program at the Erlangen University Hospital. (Ad)
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