Next Article in Journal / Special Issue
Interaction of KSHV with Host Cell Surface Receptors and Cell Entry
Previous Article in Journal
Arboviral Bottlenecks and Challenges to Maintaining Diversity and Fitness during Mosquito Transmission
Previous Article in Special Issue
Contribution of Viral Mimics of Cellular Genes to KSHV Infection and Disease
Article Menu

Export Article

Open AccessArticle
Viruses 2014, 6(10), 4005-4023; doi:10.3390/v6104005

KSHV miRNAs Decrease Expression of Lytic Genes in Latently Infected PEL and Endothelial Cells by Targeting Host Transcription Factors

1
Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA
2
UF Health Cancer Center, University of Florida, Gainesville, FL 32610, USA
3
UF Institute of Genetics, University of Florida, Gainesville, FL 32610, USA
*
Author to whom correspondence should be addressed.
Received: 9 September 2014 / Revised: 17 October 2014 / Accepted: 21 October 2014 / Published: 23 October 2014
(This article belongs to the Special Issue Kaposi's Sarcoma-Associated Herpesvirus)
View Full-Text   |   Download PDF [905 KB, uploaded 12 May 2015]   |  

Abstract

Kaposi’s sarcoma-associated herpesvirus (KSHV) microRNAs are encoded in the latency-associated region. Knockdown of KSHV miR-K12-3 and miR-K12-11 increased expression of lytic genes in BC-3 cells, and increased virus production from latently infected BCBL-1 cells. Furthermore, iSLK cells infected with miR-K12-3 and miR-K12-11 deletion mutant viruses displayed increased spontaneous reactivation and were more sensitive to inducers of reactivation than cells infected with wild type KSHV. Predicted binding sites for miR-K12-3 and miR-K12-11 were found in the 3’UTRs of the cellular transcription factors MYB, Ets-1, and C/EBPα, which activate RTA, the KSHV replication and transcription activator. Targeting of MYB by miR-K12-11 was confirmed by cloning the MYB 3’UTR downstream from the luciferase reporter. Knockdown of miR‑K12-11 resulted in increased levels of MYB transcript, and knockdown of miR-K12-3 increased both C/EBPα and Ets-1 transcripts. Thus, miR-K12-11 and miR-K12-3 contribute to maintenance of latency by decreasing RTA expression indirectly, presumably via down‑regulation of MYB, C/EBPα and Ets-1, and possibly other host transcription factors. View Full-Text
Keywords: KSHV; miRNA; lytic reactivation; latency KSHV; miRNA; lytic reactivation; latency
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Plaisance-Bonstaff, K.; Choi, H.S.; Beals, T.; Krueger, B.J.; Boss, I.W.; Gay, L.A.; Haecker, I.; Hu, J.; Renne, R. KSHV miRNAs Decrease Expression of Lytic Genes in Latently Infected PEL and Endothelial Cells by Targeting Host Transcription Factors. Viruses 2014, 6, 4005-4023.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top