Adam T. Grundhoff

This study identifies small-molecule inhibitors of BK polyomavirus infection through phenotypic screening, revealing compounds with distinct antiviral mechanisms and cellular effects.

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 that defective HIV-1 proviruses can reprogram CD4+ T cells by altering BACH2 and STAT5B gene expression, leading to immune evasion and persistence in ART-treated individuals.

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 uses human hair-bearing skin organoids to investigate HSV-1 infection and host responses, revealing cell-type-specific susceptibility and spatially organized immune reactions.

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.