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EnglishMicroRNAs 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.
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| Titolo: | Epstein-Barr virus-induced miR-155 attenuates NF-κB signaling and stabilizes latent virus persistence | |
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| Data di pubblicazione: | 2008 | |
| Rivista: | ||
| Handle: | http://hdl.handle.net/11392/2357481 | |
| Appare nelle tipologie: | 03.1 Articolo su rivista |
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