descriptionPublicationkeyboard_double_arrow_right Article , Other literature type 25 Aug 2020 English Publisher:American Society for MicrobiologyJournal:mBio, volume 11 (issn: 2161-2129, eissn: 2150-7511,

Copyright policy )Funded by:NIH | USP7 targeting by HHV-8 v..., NIH | The Robert H.Lurie Compre..., NIH | Core Essential Genes in P... +1 projects

Authors: Mark Manzano; Thomas Günther; Hyunwoo Ju; John Nicholas; Elizabeth T. Bartom; Adam Grundhoff; Eva Gottwein;

doi: 10.1128/mbio.01457-20

pmid: 32843547

pmc: PMC7448273

Kaposi’s Sarcoma-Associated Herpesvirus Drives a Super-Enhancer-Mediated Survival Gene Expression Program in Primary Effusion Lymphoma

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Abstract

Kaposi’s sarcoma-associated herpesvirus (KSHV) causes the aggressive disease primary effusion lymphoma (PEL). Here, we show that a viral transcription factor (vIRF3) cooperates with the cellular transcription factor IRF4 to control an oncogenic gene expression program in PEL cells. These proteins promote KSHV-mediated B cell transformation by activating the expression of prosurvival genes through super-enhancers. Our report thus demonstrates that this DNA tumor virus encodes a transcription factor that functions with cellular IRF4 to drive oncogenic transcriptional reprogramming.

Related Organizations

Johns Hopkins Medicine
United States
Northwestern University
United States
Heinrich-Pette-Institute
Germany
Johns Hopkins University School of Medicine
United States

Keywords

Gene Expression, KSHV, Microbiology, QR1-502, Virus Latency, Viral Proteins, HBZ, EBV, HTLV-1, IRF4, EBNA3C, Cell Line, Tumor, Lymphoma, Primary Effusion, Herpesvirus 8, Human, Interferon Regulatory Factors, Humans, Sarcoma, Kaposi, Research Article

10 Research products, page 1 of 1

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