Blood Podcast Epstein-Barr virus genomic variants in human disease states, somatic GATA1 mutations and leukemia in Down syndrome, and new definitions for high-risk multiple myeloma
Sep 25, 2025
Explore the intriguing connections between Epstein-Barr virus genomic variants and various human diseases, including hematological malignancies. Discover the timing and impact of somatic GATA1 mutations related to leukemias in individuals with Down syndrome. Dive into new high-risk definitions for multiple myeloma, focusing on crucial cytogenetic abnormalities and their implications for patient outcomes. Additionally, learn how these insights could shape future diagnostics and treatment approaches.
AI Snips
Chapters
Transcript
Episode notes
EBV Genomes Show Disease-Linked Patterns
- EBV genomes show geographically driven clustering and recurrent SNV hotspots in genes regulating latency and immune evasion.
- Large deletions and intragenic changes concentrate in hematologic cases and may upregulate viral reactivation and tumorigenesis.
Viral Transcription Factors Implicate Tumor Suppression
- Recurrent SNV hotspots occurred in EBNA-3B, EBNA-2, and LMP1, implicating transcriptional regulators in disease associations.
- EBNA-3B deletions and knockout studies suggest EBNA-3B may act as a viral tumor suppressor via host tumor suppressor regulation.
Deletions And Integration May Promote Lymphoma
- Large deletions frequently targeted viral microRNA clusters in hematologic disease, potentially promoting viral reactivation.
- EBV integration into the human genome occurred rarely but associated with tumorigenesis in sampled cases.