Epstein-Barr virus induces germinal center light zone chromatin architecture and promotes survival through enhancer looping at the BCL2A1 locus.
mBio
; 15(1): e0244423, 2024 Jan 16.
Article
em En
| MEDLINE
| ID: mdl-38059622
ABSTRACT
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.
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Base de dados:
MEDLINE
Assunto principal:
Herpesvirus Humano 4
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Proteínas Proto-Oncogênicas c-bcl-2
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Infecções por Vírus Epstein-Barr
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article