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Researchers have now discovered how the virus reactivates after lying dormant in the body. The findings could be important for long COVID research.
The first infection with a herpes virus can be unpleasant. But, it's the permanent reactivation that causes real problems.
Chickenpox is a vivid example. The cause of the itchy skin blisters is one of the nine known herpes viruses that can infect humans and make them sick: the varicella zoster virus. It is widespread all over the world and is mainly known as a children's disease. Most of the time, the little ones get over the infection fairly well, only a few scars can remain from scratching. But, the virus stays with them.
The varicella-zoster variant of the herpes virus settles in the nerve cell bodies, the so-called ganglia. It can reawaken years or decades later and come back in the form of shingles.
In addition to the varicella-zoster virus, the herpes virus family also includes the herpes simplex viruses of types 1 and 2. They are known worldwide because they are responsible for painful cold sores and genital herpes. The cytomegalovirus is also widespread and can lead to severe complications and damage to organs, especially in immuno-suppressed people.
The Epstein-Barr virus and the Kaposi's sarcoma, associated herpes virus, can cause tumors. The human herpes viruses 6 (often still subdivided into A and B) and 7 are also widespread and cause, for example, the three-day fever known as a children's disease.
"The most important thing about herpes viruses is that they remain latent in the body for a lifetime after the primary infection," says Lars Dölken, a virologist at the University of Würzburg. Dölken thus names the most important similarity of this family of viruses. Together with his colleagues he wants to understand the mechanism behind the sudden awakening of the pathogens and has taken a close look at the human herpes virus 6A (HHV-6A) for this purpose. The research team published the results in a study in the scientific journal Nature: they discovered nothing less than a previously unknown cellular mechanism by which the virus brings itself out of sleep.
People who catch a herpes virus for the first time often don't even notice it. The problem is usually the repeated reactivation of the virus. To do this, it often uses a phase in which the host's immune system is already fighting on other fronts. This can be a cold as well as strong physical and psychological stress. People with HIV or transplant patients are particularly susceptible.
HHV-6A builds itself into the genome of the human cell and survives there in the latency phase until a good opportunity presents itself for the virus to attack again and thus multiply. Then a certain microRNA gets to work and reactivates the virus.
"Almost all herpes viruses make their own micro RNAs, which are extremely important for the viruses. But there is no example of a herpes virus where the micro-RNA is so fundamental," says virologist Dölken. "If we switch off this one viral microRNA, then the virus is dead – to put it somewhat imprecisely."
MicroRNA, unlike mRNA for example, is not responsible for carrying the blueprint for certain proteins — it belongs to the non-coding RNAs. Instead, viral microRNA intervenes in the metabolism of certain human microRNAs and inhibits their development.
As a result, the production of so-called type I interferons is disturbed. These are messenger substances with which the cell signals the presence of viruses to the immune system. "But this is certainly not the only mechanism that is disturbed," says Dölken. With their investigation, the researchers had only scratched the surface, the virologist continues.
The viral microRNA makes it possible for the herpes viruses to escape the immune system, or more precisely, the B and T cells that eliminate infected human cells. "These cells recognize proteins foreign to the body — for example, those of a virus.
"However, with the help of RNA, the herpes viruses manage to reprogram the host cells and use them to their advantage without our acquired immune system, i.e. B and T cells, having a chance to recognize the cell as infected," explains Dölken.
The discovery of the one crucial viral micro-RNA, the "master regulator" as Dölken calls it, not only made it possible for the researchers to prevent the reactivation of the herpes virus in cell culture experiments.
Conversely, the findings and further research could also help in the future to reactivate latent cells in the body, which the immune system can then recognize and render harmless. "Before transplanting an organ, it would be good to be able to switch off the latent cells infected with the herpes virus," Dölken says.
The virologists in Würzburg could also contribute to solving another problem with their research: long COVID. Since herpes viruses often attack an already weakened immune system, scientists also suspect them of being involved in the various disease patterns of long COVID. "One obvious assumption is that herpes viruses are reactivated due to the corona infection, resulting in secondary damage," says Dölken. So far, there are still more questions than answers. But at least there are already a few prime suspects. HHV-6 is one of them.
This article was originally written in German.