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A step on the way to better therapies against viruses

A step towards better therapies against viruses

An electron microscope image. It shows how the herpes virus is attacked by the protein MxB. Credit: Manutea Serrero & Beate Sodeik, Virology, Hanover Medical School, Germany.

Most cells can defend themselves against viruses after they have been activated by the body’s own messenger substances (interferons). This is done with the help of proteins that recognize invading virus components and disrupt virus replication. One of these proteins is the myxovirus resistance protein B (MxB). It can inhibit many viruses, for example HIV and herpes viruses. But until now it was not clear how it does this.

Now a team led by Dr. Manutea Serrero and Professor Dr. Beate Sodeik of the Institute of Virology of the Hanover Medical School (MHH) examined new findings on the interactions between MxB and herpes viruses as part of a project of the Cluster of Excellence RESIST and published them in the journal eLife† This interdisciplinary team consists of researchers from the TU Munich, the University Hospital Freiburg, Princeton University (US) and the University of Oxford (UK). With this work, the team is on track to find new active substances for use against herpes viruses.

MxB can destroy the protection of the viruses

“Using biochemical experiments, we were able to demonstrate for the first time that MxB has the amazing ability to attack and disassemble the highly stable protective capsids of herpes viruses. The capsids enclose the genome of the viruses, protecting it from its own defenses.” the cell,” says Professor Sodeik. The work has been done with herpes simplex viruses, which cause lip and genital herpes, among other things, and with varicella zoster viruses, which cause chickenpox and shingles. Follow-up studies are now examining the effect of MxB on the capsids of other herpesviruses, for example on cytomegalovirus and Epstein-Barr virus.

So far, the team has been working with cell-free methods and with protein mixtures that are formed after cell membranes have dissolved and that contain active or mutated, inactive MxB proteins. “We are now investigating whether MxB can also decompose the capsids in intact, infected cells and in which cell types this mechanism is activated by the interferons,” explains Professor Sodeik.

To this end, the team is developing methods to produce virus particles in which both the capsids and the viral genomes are labeled. MxB-containing cells are then infected with these viruses and examined at which stages of the infection cycle the cell protein MxB attacks the labeled capsids and whether the labeled genomes are released from the disassembled capsids. “A better molecular understanding of this interferon-induced defense mechanism against herpes viruses may be used to develop new treatments against herpes viruses that attack capsids,” said the researcher.


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More information:
Manutea C Serrero et al, The interferon-inducible GTPase MxB promotes capsid disassembly and genome delivery of herpesviruses, eLife (2022). DOI: 10.7554/eLife.76804

Journal information:
eLife


Provided by Medizinische Hochschule Hannover

Quote: A Step Towards Better Therapies Against Viruses (2022, July 1), retrieved July 2, 2022 from https://phys.org/news/2022-07-therapies-viruses.html

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