Viral-associated cancers and disorders

The paper uses mathematical models to analyze HHV-8 oral shedding patterns in Ugandan individuals, finding that shedding rates depend on reactivation rates and immune responses.

This study identifies viral lncRNAs that regulate EBV reactivation by interacting with CTCF and modulating enhancer-promoter looping.

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 creates the first multiomic single-cell spatial atlas of palatine tonsils in infectious mononucleosis, revealing EBV's epithelial tropism and immunosuppressive microenvironment.

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.

This study performs a single-cell transcriptomic analysis of EBV-responsive lymphocytes in healthy and immunodeficient individuals, identifying key immune mechanisms and potential therapeutic targets.

This study shows that viral IL-6 (vIL-6) and human IL-6 work together to influence cytokine expression and immune responses during KSHV infection.

This study maps EBV-induced genomic variations and identifies MUC19 as an oncogenic factor promoting latency through mTOR activation.

This study identifies RIG-I deficiency as a cause of classic Kaposi sarcoma by impairing control of KSHV infection and reactivation.

This study identifies ORF29 as a critical component of the KSHV terminase complex, essential for capsid formation and TR cleavage, and shows it interacts with itself and ORF7.

This paper presents a spatial single-cell atlas of Kaposi's sarcoma, identifying CD34+ progenitor lymphatic endothelial cells as primary targets of KSHV and revealing mechanisms of tumor progression and immune modulation.

This paper uses long-read RNA-seq to analyze EBV transcriptomes in LCLs, identifying new splicing variants, polyA sites, and transcript structures, and provides tools and annotations for future studies.

The paper identifies EBV-associated methylation patterns in breast cancer and normal tissues that align with stem cell differentiation pathways, suggesting EBV contributes to cancer susceptibility through epigenetic changes.

The paper uses population-scale whole genome sequencing to identify EBV DNA as a biomarker for respiratory, autoimmune, and cardiovascular diseases and identifies genetic determinants of EBV persistence.

This study investigates why XLP-2 patients, with XIAP deficiency, avoid EBV-driven lymphoma despite severe EBV infection, finding that XIAP loss impairs EBV-induced B-cell outgrowth and promotes apoptosis.

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

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.

The paper investigates EBNA-1 specific antibodies in IM patients, finding persistent functional antibodies with cross-reactivity to CRYAB and association with MS risk alleles.

This study shows HSF2 promotes gamma-herpesvirus lytic gene expression by altering chromatin structure at key viral promoters.

This study identifies K5 as a KSHV protein cleaved by caspases during lytic replication, which helps protect infected cells from apoptosis.

This study quantifies morphological and mechanical changes in endothelial cells infected with KSHV, identifying potential diagnostic and therapeutic markers.

This study uses single-cell RNA sequencing to analyze Kaposi Sarcoma tumors and blood samples, identifying KSHV-infected cell types and their biomarkers, and showing changes with therapy.

This study investigates how KSHV terminal repeats (TR) function as enhancers by regulating BRD4 recruitment and promoter activation during viral reactivation.

This study identifies a GC-rich cis element in the ORF75 promoter of KSHV that drives its constitutive expression in endothelial and epithelial cells, contributing to its high expression in Kaposi sarcoma lesions.

This paper uses long-read RNA sequencing to create a comprehensive transcriptomic atlas of Caviid Gammaherpesvirus 1, revealing its transcriptome and regulatory mechanisms.

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.

The paper identifies differential EBV protein-specific antibody responses between responders and non-responders to EBVST immunotherapy, suggesting these antibodies could predict clinical outcomes.

This paper identifies that EBV's BALF0/1 protein degrades B-cell receptor complexes by subverting caveolin and ERAD pathways, enhancing viral secretion.

This study identifies E2F1 as a suppressor of EBV lytic reactivation by regulating transcriptional networks involving BZLF1 and c-Myc.