Micah A. Luftig

The paper assesses EBV dependence in various infected cell models and finds that EBV loss sensitivity varies across cell types, with lymphoid malignancies being more dependent than gastric adenocarcinoma lines.

This study uses spatial transcriptomics to show that EBV+ HIV-associated NHLs have distinct tumor microenvironment features, including immunosuppressive pathways and spatial organization similar to lymphoid tissues.

This study uses single-cell RNA sequencing to analyze the effects of HDAC inhibitors on EBV lytic reactivation in B lymphoblasts, identifying abortive and refractory states.

The paper identifies Sp140L as a novel restriction factor that herpesviruses counteract to evade innate immune responses and establish infection.

This study identifies fatty acid desaturases SCD1 and FADS2 as critical for EBV-induced B cell proliferation and reveals their role in promoting metabolic pathways that support lymphoma growth.

The paper identifies FCRL3 as a receptor for Yersinia pestis using a genome-wide association study and shows a variant in FCRL3 is linked to both plague susceptibility and hepatitis C risk.

This study uses single-cell transcriptomics to analyze EBV lytic reactivation in B cells, revealing abortive, reprogrammed, and host shutoff states with distinct gene expression patterns.

This study identifies EBNA-LP's role in promoting naive B cell transformation by interacting with YY1 through conserved leucine-rich motifs.

The paper identifies EBV variants, particularly in LMP1, associated with survival in Burkitt lymphoma and defines prognostic subgroups based on these features.

The paper analyzes EBV genomes from eBL patients and controls in Kenya, finding type 1 EBV is more common in patients and identifying genetic variants associated with eBL.