Epstein-Barr virus growth/latency III program alters cellular microRNA expression

Virology. 2008 Dec 20;382(2):257-66. doi: 10.1016/j.virol.2008.09.018. Epub 2008 Oct 31.


The Epstein-Barr virus (EBV) is associated with lymphoid and epithelial cancers. Initial EBV infection alters lymphocyte gene expression, inducing cellular proliferation and differentiation as the virus transitions through consecutive latency transcription programs. Cellular microRNAs (miRNAs) are important regulators of signaling pathways and are implicated in carcinogenesis. The extent to which EBV exploits cellular miRNAs is unknown. Using micro-array analysis and quantitative PCR, we demonstrate differential expression of cellular miRNAs in type III versus type I EBV latency including elevated expression of miR-21, miR-23a, miR-24, miR-27a, miR-34a, miR-146a and b, and miR-155. In contrast, miR-28 expression was found to be lower in type III latency. The EBV-mediated regulation of cellular miRNAs may contribute to EBV signaling and associated cancers.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • B-Lymphocytes / metabolism
  • B-Lymphocytes / virology
  • Base Sequence
  • Cell Line
  • Cell Transformation, Viral
  • DNA Primers / genetics
  • Gene Expression
  • Gene Expression Profiling
  • Herpesvirus 4, Human / genetics
  • Herpesvirus 4, Human / pathogenicity*
  • Herpesvirus 4, Human / physiology
  • Humans
  • MicroRNAs / genetics*
  • RNA, Viral / genetics
  • Signal Transduction
  • Virus Latency / genetics
  • Virus Latency / physiology


  • DNA Primers
  • MicroRNAs
  • RNA, Viral