Viral-associated cancers and disorders

This study uses RNA-seq to analyze gene expression in EBV-positive and EBV-negative gastric cancer samples, identifying differentially expressed genes and viral gene activity associated with tumor progression.

The paper identifies miR-31-5p as a regulator of KSHV lytic reactivation by targeting KHDRBS3, reducing viral gene expression and infectious virion production.

This study shows that a replication-dead murine gammaherpesvirus lacking pathogenesis genes can protect against wild-type virus infection by inducing neutralizing antibodies and CD8 T-cell responses.

This study identifies KSHV ORF57 as a viral RNA-binding protein that stabilizes FOS RNA, inhibits AEN, and transactivates RGS2 to promote AKT phosphorylation during lytic infection.

This paper evaluates limitations in EBV detection protocols for breast cancer studies in the US, finding that many assays use outdated or mismatched sequences, potentially skewing results.

This study shows that glycoprotein K8.1 is critical for KSHV tissue tropism in marmosets, but not for initial infection.

This study uses cryoET and deep learning to reveal structural differences in the tegument and envelope of EBV and KSHV virions compared to other herpesviruses.

This study uses large language models to analyze EBV-related publications, identifying key antigens and pathways involved in EBV-mediated diseases and validating their roles in specific cancers.

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 shows that WAPL suppresses LMP1 and LMP2A expression in EBV latency I by altering DNA looping and histone marks, preventing the transition to latency II.

This study shows ORF48 is essential for KSHV lytic replication by inhibiting the cGAS-STING pathway and blocking innate immune signaling.

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 miR-142 as a regulator of EBV reactivation through CRISPR/Cas9 screening and shows it suppresses SOS1/Ras/Raf/Mek/Erk signaling initiated by the BCR.

This paper shows that combining bortezomib and venetoclax kills PTLD cells by targeting EBV proteins LMP-1 and EBNA-3C through proteasome inhibition and Bcl-2 suppression.

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

This study identifies constitutive and lytically induced enhancers in the KSHV genome using functional assays and CRISPR techniques, revealing a 'viral super-enhancer' that regulates latency-to-lytic transition.

The paper identifies KSHV- and HIV-specific T-cells in KS tumors and shows they persist over time and coexist with immunosuppressive macrophages.

This study shows that bleomycin induces apoptosis in EBV-infected gastric epithelial cells via a DNA damage response, and LMP2A enhances this effect by promoting DDR.

The paper uses electron microscopy to map DNA-binding sites of KSHV RTA protein and identifies its oligomeric states when bound to viral DNA.

The paper shows EBV infections disable breast cancer safeguards, leading to similar genetic and molecular patterns as hereditary breast cancers.

The paper identifies ORF29 as a viral DNA packaging motor subunit that potentiates late gene expression in KSHV, linking transcription and packaging processes.

This study identifies how EBNA2 interacts with EBF1 to drive MYC expression and metabolic processes necessary for cell cycle progression in EBV-infected B cells.

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.

The paper investigates how human genetic variation influences Epstein-Barr virus (EBV) sequence diversity by analyzing paired viral and human genomic data from HIV-coinfected individuals.

This study identifies a genetic variant near CXCL12 associated with increased susceptibility to HIV-related non-Hodgkin lymphoma.

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.

The paper identifies miR-141 and EBV miR-BART9 as regulators of B cell reactivation through FOXO3 inhibition, linking BCR signaling to lytic replication in EBV.

This paper identifies conserved CxnC motifs in KSHV ORF66 essential for its interaction with ORF34 and late gene expression.

The paper identifies two EBV variants in BALF2 associated with increased NPC risk through genome sequencing and association studies in China.

This study identifies the critical role of the ORF18-ORF30 interaction in KSHV late gene expression through mutational analysis.