Epstein-Barr virus-induced miR-155 attenuates NF-κB signaling and stabilizes latent virus persistence

MicroRNAs have been implicated in the modulation of gene expression programs important for normal and cancer cell development. miR-155 is known to play a role in B-cell development and is upregulated in various B-cell lymphomas, including several that are latently infected with Epstein-Barr virus (EBV). We show here that EBV infection of primary human B lymphocytes leads to the sustained elevation of miR-155 and its precursor RNA, BIC. The EBV-encoded latency membrane protein 1 (LMP1) can partially reconstitute BIC activation in B lymphocytes but not in epithelial cell cultures. LMP1 is a potent activator of NF-κB signaling pathways and is essential for EBV immortalization of B lymphocytes. An inhibitor to miR-155 further stimulated NF-κB responsive gene transcription, and IKKε was identified as a potential target of miR-155 translational repression. Remarkably, miR-155 inhibitor reduced EBNA1 mRNA and the EBV copy number in latently infected cells. This suggests that miR-155 contributes to EBV immortalization by modulation of NF-κB signaling and the suppression of host innate immunity to latent viral infection. Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Data di pubblicazione: 2008
Titolo: Epstein-Barr virus-induced miR-155 attenuates NF-κB signaling and stabilizes latent virus persistence
Autori: Lu, Fang; Weidmer, Andreas; Liu, Chang-Gong; Volinia, Stefano; Croce, Carlo M.; Lieberman, Paul M.
Rivista: JOURNAL OF VIROLOGY
Parole Chiave: Immunology; Virology
Abstract in inglese: MicroRNAs have been implicated in the modulation of gene expression programs important for normal and cancer cell development. miR-155 is known to play a role in B-cell development and is upregulated in various B-cell lymphomas, including several that are latently infected with Epstein-Barr virus (EBV). We show here that EBV infection of primary human B lymphocytes leads to the sustained elevation of miR-155 and its precursor RNA, BIC. The EBV-encoded latency membrane protein 1 (LMP1) can partially reconstitute BIC activation in B lymphocytes but not in epithelial cell cultures. LMP1 is a potent activator of NF-κB signaling pathways and is essential for EBV immortalization of B lymphocytes. An inhibitor to miR-155 further stimulated NF-κB responsive gene transcription, and IKKε was identified as a potential target of miR-155 translational repression. Remarkably, miR-155 inhibitor reduced EBNA1 mRNA and the EBV copy number in latently infected cells. This suggests that miR-155 contributes to EBV immortalization by modulation of NF-κB signaling and the suppression of host innate immunity to latent viral infection. Copyright © 2008, American Society for Microbiology. All Rights Reserved.
Digital Object Identifier (DOI): 10.1128/JVI.00752-08
Handle: http://hdl.handle.net/11392/2357481
Appare nelle tipologie:03.1 Articolo su rivista

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