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  • Meeting abstract
  • Open Access

Cloned HTLV-1+CD4+, but not CD8+, T-cells display an oncogenic miRNome

  • 1,
  • 2,
  • 3,
  • 1,
  • 3 and
  • 1Email author
Retrovirology20118 (Suppl 1) :A169

https://doi.org/10.1186/1742-4690-8-S1-A169

  • Published:

Keywords

  • Transcriptome Data
  • Clonal Expansion
  • Cell Cycling
  • Prominent Effect
  • Untransformed Cell

HTLV-1 persistence in vivo relies on the persistent clonal expansion of its host cells. These are CD4+ and CD8+ T cells, yet ATL is regularly CD4+. Accordingly, untransformed HTLV-1+CD4+ but not CD8+ T cells cloned from carriers cumulate the features of preleukemic cells, including multinuclearity, chromatin bridges, increased cell cycling and inappropriate telomerase activity. MicroRNAs (miR) modify the maturation of a plethora of T-cells RNA and their deregulation would therefore constitute an appropriate explanation for the Tax-dependent or -independent pleiotropic changes in the phenotype of HTLV-1+CD4+ T cells. As the miRNome of naturally infected untransformed cells has not been investigated to date, we assessed the miR expression profiling of T cells cloned from carriers. Microarray results, confirmed by quantitative RTPCR, showed that, upon infection, CD4+ and CD8+ clones yielded aberrant expression of 15 distinct miRs including miR-34b and miR-494 that were respectively over- and underexpressed in both compartments. The more prominent effect of the infection consisted in the CD4+-restricted overexpression of the cancer-related miRs miR-21, -27b and -23b associated with the CD4+-restricted downregulation of the proapoptotic miR-15 and -16. Data were extended by the analysis of 40 additional CD4+ clones (20 infected). Crossing the miRNome against the whole transcriptome data identified putative miR-targeted genes. In silico, those targeted by miR-23b and -27b defined 2 hitherto unknown pathways involving the cell cycle and genetic disorders. Therefore HTLV-1 triggers a phenotype-specific miR signature consistent with the preleukemic HTLV-1+CD4+ phenotype.

Authors’ Affiliations

(1)
Oncovirologie et de Biotherapies, UMR5239 CNRS/ENS Lyon/UCBL/HCL, Hopital Pierre Benite, Lyon, France
(2)
Oncovirologie et de Biotherapies, Centre Léon Berard, Lyon, France
(3)
ProfileXpert, Neurobiotec Service, Bron, 69500, France

Copyright

© Vernin et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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