Epstein-Barr virus induces germinal center light zone chromatin architecture and promotes survival through enhancer looping at the BCL2A1 locus.

Autor:	Dai J; Department of Molecular Genetics and Microbiology, Center for Virology, Duke University School of Medicine, Durham, North Carolina, USA., SoRelle ED; Department of Molecular Genetics and Microbiology, Center for Virology, Duke University School of Medicine, Durham, North Carolina, USA., Heckenberg E; Department of Molecular Genetics and Microbiology, Center for Virology, Duke University School of Medicine, Durham, North Carolina, USA., Song L; Center for Genomic & Computational Biology, Duke University, Durham, North Carolina, USA.; Division of Medical Genetics, Department of Pediatrics, Duke University, Durham, North Carolina, USA., Cable JM; Department of Molecular Genetics and Microbiology, Center for Virology, Duke University School of Medicine, Durham, North Carolina, USA., Crawford GE; Center for Genomic & Computational Biology, Duke University, Durham, North Carolina, USA.; Division of Medical Genetics, Department of Pediatrics, Duke University, Durham, North Carolina, USA., Luftig MA; Department of Molecular Genetics and Microbiology, Center for Virology, Duke University School of Medicine, Durham, North Carolina, USA.
Jazyk:	angličtina
Zdroj:	MBio [mBio] 2024 Jan 16; Vol. 15 (1), pp. e0244423. Date of Electronic Publication: 2023 Dec 07.
DOI:	10.1128/mbio.02444-23
Abstrakt:	Importance: Epstein-Barr virus has evolved with its human host leading to an intimate relationship where infection of antibody-producing B cells mimics the process by which these cells normally recognize foreign antigens and become activated. Virtually everyone in the world is infected by adulthood and controls this virus pushing it into life-long latency. However, immune-suppressed individuals are at high risk for EBV+ cancers. Here, we isolated B cells from tonsils and compare the underlying molecular genetic differences between these cells and those infected with EBV. We find similar regulatory mechanism for expression of an important cellular protein that enables B cells to survive in lymphoid tissue. These findings link an underlying relationship at the molecular level between EBV-infected B cells in vitro with normally activated B cells in vivo . Our studies also characterize the role of a key viral control mechanism for B cell survival involved in long-term infection. Competing Interests: The authors declare no conflict of interest.
Databáze:	MEDLINE
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