Regulation of interleukin-1β transcription by Epstein-Barr virus involves a number of latent proteins via their interaction with RBP

Krauer, Kenia G., Belzer, Deanna K., Liaskou, Daphne, Buck, Marion, Cross, Simone, Honjo, Tasuku and Sculley, Tom (1998) Regulation of interleukin-1β transcription by Epstein-Barr virus involves a number of latent proteins via their interaction with RBP. Virology, 252 2: 418-430. doi:10.1006/viro.1998.9441


Author Krauer, Kenia G.
Belzer, Deanna K.
Liaskou, Daphne
Buck, Marion
Cross, Simone
Honjo, Tasuku
Sculley, Tom
Title Regulation of interleukin-1β transcription by Epstein-Barr virus involves a number of latent proteins via their interaction with RBP
Journal name Virology   Check publisher's open access policy
ISSN 0042-6822
1096-0341
Publication date 1998-12-20
Sub-type Article (original research)
DOI 10.1006/viro.1998.9441
Volume 252
Issue 2
Start page 418
End page 430
Total pages 13
Place of publication Maryland Heights, MO, United States
Publisher Academic Press
Language eng
Abstract Epstein–Barr virus (EBV) infects B cells, resulting in the outgrowth of immortalised lymphoblastoid cell lines (LCLs). Here, we demonstrate through the use of intracellular staining that interleukin-1β (IL-1β) is expressed in LCLs and investigate the influence of the individual latent proteins on the expression of IL-1β. Using RT-PCR, IL-1β was shown to be up-regulated in EBV-transformed LCLs as well as in group III Burkitt's lymphoma (BL) cell lines, compared with group I BL cell lines. The up-regulation of IL-1β message could be mediated by the latent membrane protein-1, EBV nuclear proteins 2, 3, 4, and 6 genes. Electrophoretic mobility shift assays (EMSAs) demonstrated that the −300 region of the IL-1β promoter, which contains a nuclear factor-κB (NF-κB) binding site, contained a functional RBP binding site. Binding of RBP to this site could be inhibited by addition of EBV nuclear proteins 3 and 6, suggesting that these proteins displace RBP from its recognition sequence, removing transcriptional repression and allowing gene transcription to occur. In group I BL cells, containing low levels of NF-κB, only RBP binding was observed in EMSAs, whereas NF-κB binding could be demonstrated in EBV-transformed B cell lines containing high levels of activated NF-κB. In addition, the expression of latent membrane protein-1 led to activation of NF-κB that was capable of binding the IL-1β promoter. The study demonstrates that EBV can up-regulate IL-1β expression, possibly by using RBP, NF-κB, or both.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
 
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Created: Wed, 19 Oct 2011, 12:21:42 EST by Marion Buck on behalf of Royal Brisbane Clinical School