Thomas Günther

This study maps the molecular changes in murine upper-layer cortical neurons during development and shows how maternal immune activation disrupts this process through post-transcriptional and signaling mechanisms.

This study shows KSHV uses SOX18 to maintain viral episomes in LECs by enhancing chromatin accessibility.

This paper demonstrates that iPSC-derived skin organoids support MCPyV infection, persistence, and tumor development, providing a model to study viral interactions with the immune system and treatment strategies.

This study develops a CRISPR/Cas9-based 3D live cell imaging system to track KSHV episomes in real-time, revealing their spatiotemporal dynamics during infection.

This study shows that Polycomb group proteins maintain KSHV latency by repressing viral gene expression and protecting episomes from HUSH-dependent silencing.

This study investigates VZV gene repression in neuronal cells, finding that histone deposition is absent at quiescent viral genomes.

This study identifies the HUSH complex as a host factor that restricts HAdV infection through epigenetic silencing, and shows HAdV proteins inhibit this complex to promote viral replication.

This study identifies SUMOylation of HAdV E2A/DBP as a mechanism to inhibit p53 activity and apoptosis, revealing a novel pathway for viral oncogenic potential.

This study shows that HPV18 infection reprograms host transcription by altering CTCF binding and promoter-enhancer interactions, leading to repression of the tumor suppressor CADM1.

This study identifies a novel function of MCPyV small T antigen in suppressing the type I interferon response by reducing IRF9 levels, impacting immune evasion and tumor progression.

This paper identifies M35 as a viral protein that binds DNA and inhibits IRF3-mediated gene expression, including Ifnb1, thereby suppressing the antiviral type I IFN response.

This study identifies two MCPyV integration patterns in MCC and links them to NHEJ and MMBIR mechanisms, showing integration preference for open chromatin and viral promoter-driven oncogene expression.