Epstein-Barr virus maintains lymphomas via its miRNAs

D. T. Vereide, E. Seto, Y. F. Chiu, M. Hayes, T. Tagawa, A. Grundhoff, W. Hammerschmidt, B. Sugden*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

129 Scopus citations

Abstract

Epstein-Barr virus (EBV) has evolved exquisite controls over its host cells, human B lymphocytes, not only directing these cells during latency to proliferate and thereby expand the pool of infected cells, but also to survive and thereby persist for the lifetime of the infected individual. Although these activities ensure the virus is successful, they also make the virus oncogenic, particularly when infected people are immunosuppressed. Here we show, strikingly, that one set of EBV's microRNAs (miRNAs) both sustain Burkitt's lymphoma (BL) cells in the absence of other viral oncogenes and promote the transformation of primary B lymphocytes. BL cells were engineered to lose EBV and found to die by apoptosis and could be rescued by constitutively expressing viral miRNAs in them. Two of these EBV miRNAs were found to target caspase 3 to inhibit apoptosis at physiological concentrations.

Original languageEnglish
Pages (from-to)1258-1264
Number of pages7
JournalOncogene
Volume33
Issue number10
DOIs
StatePublished - 03 2014
Externally publishedYes

Keywords

  • BART miRNAs
  • Burkitt's lymphoma
  • EBV
  • RISC-IP
  • apoptosis

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