Publications by authors named "Katarzyna Szymanska-de Wijs"
Article Synopsis
- Cytomegaloviruses (CMVs) spread mainly through cell-to-cell transfer, which involves altering cellular signaling and structure.
- The viral particles transfer genetic material as well as specific proteins that help the virus evade the host's immune defenses right after infection.
- The study highlights the UL25 gene family of CMVs, focusing on how M25 proteins from mouse CMV disrupt the p53 tumor suppressor's antiviral effects and reorganize the cytoskeleton in infected cells.
To ensure productive infection, herpesviruses utilize tegument proteins and nonstructural regulatory proteins to counteract cellular defense mechanisms and to reprogram cellular pathways. The M25 proteins of mouse cytomegalovirus (MCMV) belong to the betaherpesvirus UL25 gene family that encodes viral proteins implicated with regulatory functions. Through affinity purification and mass spectrometric analysis, we discovered the tumor suppressor protein p53 as a host factor interacting with the M25 proteins.
View Article and Find Full Text PDFEbolaviruses continue to inflict horrific disease and instill fear. The 2013-2016 outbreak in Western Africa caused unfathomable morbidity and mortality (over 11,000 deaths), and the second largest outbreak is on-going in the Democratic Republic of the Congo. The first stage of an Ebolavirus infection is entry, culminating in delivery of the viral genome into the cytoplasm to initiate replication.
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