Sabrina Schreiner holds the W2 RESIST professorship for virus replication in cellular chromatin at the MHH Institute of Virology since October 2020. She focuses with her research on human adenoviruses, which cause conjunctivitis, gastrointestinal disorders or pneumonia, among other things.

In most cases, such a disease proceeds in healthy adults either without any clear or with very mild symptoms. “It can be assumed that everyone has already had several adenovirus infections,” explains Professor Schreiner. The human adenovirus, of which there are currently more than 85 different types known, were previously not considered particularly dangerous. But in immunocompromised people, the infection can become severe and even fatal. The disease is particularly dangerous for children after a stem cell transplantation.

“Since 2006, it has also been known that infections with adenoviruses can cause severe pneumonia in healthy people as well, which can have fatal consequences. We do not yet understand the molecular background in detail,” says Professor Schreiner. So far, there is no drug that is specifically effective against adenoviruses. There are also no vaccinations for the healthy population.

Professor Schreiner investigates together with her team how the virus multiplies in the cell. “We have observed that an adenovirus infection causes a significant change of so-called PML core bodies in the cell, a complex of several proteins,” she says. The otherwise round structures dissolve and elongated fibrils are formed. “It is suspected that the PML core bodies have an antiviral function – not only in human adenoviruses,” explains the 38-year-old Sabrina Schreiner.

“Adenoviruses destroy the round structures of the protein complexes and then use this manipulation of the cell for their own reproduction,” Professor Schreiner describes. Her team is therefore working on an antiviral agent that acts against these cell structures and not directly against the virus. This is because viruses often develop resistance to drugs that target them directly. For example, they can mutate so that they are no longer recognised by the drug.

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