Eric M. Burton

This study identifies arginine metabolism as critical for maintaining Epstein-Barr virus latency by supporting de novo pyrimidine biosynthesis, and shows that restricting arginine or disrupting pyrimidine synthesis can induce EBV reactivation.

This study identifies JunB as a key dependency factor in EBV-infected B cells that represses p18INK4c, revealing a potential therapeutic target for EBV-associated cancers.

This paper identifies STEEP1 as a host factor critical for LMP1 trafficking and signaling using a CRISPR-Cas9 screen, showing its role in NF-kB and MAP kinase pathway activation.

This study shows that EBV's LMP1 protein prevents ferroptosis by enhancing glutathione and NADPH through the pentose phosphate pathway and cystine uptake.

This study identifies LMP1-driven metabolic reprogramming in B-cells, showing that IMPDH inhibition sensitizes EBV-transformed cells to apoptosis, suggesting therapeutic targets for LMP1-driven lymphomas.