Paul M. Lieberman

This study shows that NAD metabolism supports CTCF-cohesin chromatin regulation in EBV-transformed B-cells and identifies NAMPT inhibition as a potential therapeutic strategy.

This study identifies RSAD2 and CMPK2 as key regulators of EBV reactivation and host interferon responses, revealing their coordinated immunometabolic role in viral latency and immune control.

ERVmancer is a phylogeny-informed method that resolves read-mapping ambiguity for HERVs, outperforming existing approaches and revealing new biology in breast cancer.

This study identifies CDC7 and POU2F1 as direct targets of EBNA1 in EBV+ epithelial cancers using VK1727 inhibition, revealing new therapeutic strategies.

The paper investigates the effects of decitabine on EBV-associated gastric cancer by integrating transcriptomic and methylome data, revealing retinoic acid pathway activation as a potential therapeutic target.

The paper identifies P2RX5 as a new B-cell surface marker and multi-lineage immunotherapy target, showing its expression in B-cell malignancies and T-cell leukemia, and demonstrating the efficacy of P2RX5-directed therapies.

This study shows lamin A/C maintains genome structure and transcriptional programs needed for EBV-driven B cell activation, with loss causing chromatin reorganization and gene expression changes.

This study uses an ex vivo PBMC model to show that monocyte and Treg dynamics determine EBV infection outcomes, with LIPA and Tregs playing key roles in antiviral responses and LCL outgrowth.

The paper shows LANA binding at KSHV TRs causes R-loops and histone modifications linked to episome maintenance.

This study shows H2A.Z.1 works with EBNA1 to maintain EBV latency by regulating chromatin structure and gene expression.

The paper develops viRNAtrap, a deep learning-based pipeline to identify and characterize viral expression in cancer, revealing new viruses and endogenous viruses linked to poor survival.

This study identifies PLOD1 as a post-translational regulator of EBNA1 protein stability and function in EBV latency, showing that PLOD1 depletion reduces EBNA1 levels and inhibits viral replication and episome maintenance.