Humans have eight different herpes viruses. They all stay in the body after an illness. Under certain circumstances, they wake up and start attacking other cells. Symptoms of this reactivation include itchy cold sores or shingles.
In the course of evolution, most herpesviruses have learned to reprogram their host cells. A research team led by Bhupesh Prusty and Lars Dölken from Julius-Maximilians-Universität (JMU) Würzburg in Germany has been able to show for the first time. In the journal Nature, the researchers present the previously unknown cellular mechanism by which human herpesviruses 6 (HHV-6) awakens.
There were problems after the reactivation of the virus.
Most people don't know they'reinfecting with HHV 6. The virus only causes problems when it wakes up many times.
Multiplesclerosis or chronic fatigue syndrome are diseases caused by the rejection of transplant organs and the impairing of heart function. Recent studies suggest that the herpesviruses may be involved in the development of diseases of the nervous system.
The central question in herpesviruses research is how to reactivate from a dormant state. The reactivation of HHV6 is initiated by the central switch.
What does the microRNA do in the cell?
The regulatory miR-aU14 comes from the virus. It affects the metabolism of human microRNAs as soon as it is expressed. It interfered with the maturation of several microRNAs. The important cellular microRNAs are no longer being produced. The so-called miR-30 / p53 / Drp1 axis is affected by this.
The viral miR-aU14 causes the breakdown of the mitochondria. These cell structures are important for energy production and signal transmissions in the defense against viruses.
The production of type I interferons is affected by the production of the viral miR-aU14 The herpesviruses can switch from a dormant to an active state without the help of the interferons. The research group was able to show that the viral microRNA is essential for virus replication and reactivation, and that it also causes the reactivation of the virus from its dormant state.
The research continues.
The researchers want to understand the mechanism by which the viral microRNA causes the reactivation of the virus. There are indications that other herpesviruses can be reactivated as well. This could show us how to prevent reactivation of these viruses or how to specifically cause it in order to eliminate the reactivating cells. The goal is to understand the consequences of mitochondrial breakdown in detail.
This is the first time that a microRNA can regulate the maturation process of other microRNAs. Artificial smallRNAs can be designed to specifically switch off individual members of microRNA families. It was not possible to make subtle interventions.
The partners and sponsors of the project.
Several groups at JMU are doing research on this topic. They are from the Institute of Virology and Immunobiology, the Biocentres, the Chairs of Biochemistry, Biotechnology and Biophysics, and the Rudolf Virchow Centre. The University of Regensburg and the Free University of Berlin were involved.
The research was funded by the European Research Council, the Solve ME/CFS Initiative, the HHV6 Foundation, and the Helmholtz Institute.
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The materials were provided by the University of rzburg. Robert Emmerich wrote the original. Content can be edited for style and length.