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Journal of Virology, June 2008, p. 5295-5306, Vol. 82, No. 11
0022-538X/08/$08.00+0     doi:10.1128/JVI.02380-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

MicroRNA-155 Is an Epstein-Barr Virus-Induced Gene That Modulates Epstein-Barr Virus-Regulated Gene Expression Pathways{triangledown} ,{dagger}

Qinyan Yin,1,2,3 Jane McBride,3 Claire Fewell,3 Michelle Lacey,4 Xia Wang,3 Zhen Lin,1,2,3 Jennifer Cameron,1,2 and Erik K. Flemington1,2,3*

Louisiana Cancer Research Consortium,1 Tulane Cancer Center,2 Department of Pathology,3 Department of Mathematics, Tulane University, New Orleans, Louisiana4

Received 2 November 2007/ Accepted 13 March 2008

The cellular microRNA miR-155 has been shown to be involved in lymphocyte activation and is expressed in Epstein-Barr virus (EBV)-infected cells displaying type III latency gene expression but not type I latency gene expression. We show here that the elevated levels of miR-155 in type III latency cells is due to EBV gene expression and not epigenetic differences in cell lines tested, and we show that expression in EBV-infected cells requires a conserved AP-1 element in the miR-155 promoter. Gene expression analysis was carried out in a type I latency cell line transduced with an miR-155-expressing retrovirus. This analysis identified both miR-155-suppressed and -induced cellular mRNAs and suggested that in addition to direct targeting of 3' untranslated regions (UTRs), miR-155 alters gene expression in part through the alteration of signal transduction pathways. 3' UTR reporter analysis of predicted miR-155 target genes identified the transcriptional regulatory genes encoding BACH1, ZIC3, HIVEP2, CEBPB, ZNF652, ARID2, and SMAD5 as miR-155 targets. Western blot analysis of the most highly suppressed of these, BACH1, showed lower expression in cells transduced with a miR-155 retrovirus. Inspection of the promoters from genes regulated in EBV-infected cells and in cells infected with an miR-155 retrovirus identified potential binding sequences for BACH1 and ZIC3. Together, these experiments suggest that the induction of miR-155 by EBV contributes to EBV-mediated signaling in part through the modulation of transcriptional regulatory factors.

* Corresponding author. Mailing address: Tulane University Health Sciences Center, 1430 Tulane Ave., SL79, New Orleans, LA 70112. Phone: (504) 988-1167. Fax: (504) 988-5516. E-mail: eflemin{at}tulane.edu

{triangledown} Published ahead of print on 26 March 2008.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, June 2008, p. 5295-5306, Vol. 82, No. 11
0022-538X/08/$08.00+0     doi:10.1128/JVI.02380-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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