Volume 11 Supplement 1

16th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access

MicroRNAs expression in CD4 T cells from HTLV-1 individuals

  • Kátia Kaori Otaguiri1,
  • Mariana Tomazini Pinto1, 2,
  • Evandra Strazza Rodrigues1, 2,
  • Virgínia Mara de Deus Wagatsuma1,
  • Maurício Cristiano Rocha Júnior1, 2,
  • Osvaldo Massaiti Takayanagui3,
  • Dimas Tadeu Covas1, 3 and
  • Simone Kashima1, 2
Retrovirology201411(Suppl 1):P111

https://doi.org/10.1186/1742-4690-11-S1-P111

Published: 7 January 2014

HAM/TSP is an inflammatory manifestation of central nervous system caused by HTLV-1 and the mechanism of HAM/TSP development is no well elucidated. Currently, a promising approach on the physiopathogenesis of viral infections has been the evaluation of microRNAs (miRNAs) role. There are few data involving CD4+ T cells miRNA expression in HTLV-1 infection as well as in HAM/TSP establishment. To identify miRNAs differentially expressed in CD4+ T cells among non-infected individuals (CT), asymptomatic (HAC) and HAM/TSP patients we applied quantitative real time PCR. The analysis of miRNA expression profile in these cells showed 56 and 10 miRNAs upregulated 1.5 times in HAM/TSP and HAC groups, respectively. miR-125b-1-1 was upregulated in HAC group and miR-146a in HAM/TSP. Target prediction by in silico analysis showed that IFNG was a potentially miR-125b-1-1 target and IRAK1 and TRAF6 were miR-146a targets. IFNG expression was 1.3 higher in HAC than CT group and 1.8 higher in HAM/TSP than CT group. It was observed that TRAF6 expression was 15.7 and 1.5 times higher in HAM/TSP and HAC groups, respectively. There was no difference of IRAK1 expression among the three groups. Overexpression assays of miR-125b-1-1 altered IFNG expression and overexpression of miR-146a altered IRAK1 gene and protein expression. The results revealed that miRNAs could modulate genes and proteins during HTLV-1 infection. miR-125b and IFNG gene correlation suggests that miR-125b seems to contribute to HAM/TSP development. Besides, interaction between miR-146a and IRAK1/TRAF6 suggests that miR-146a seems to contribute to HTLV-1 establishment in CD4+ T cells.

Authors’ Affiliations

(1)
Regional Blood Center of Ribeirão Preto, University of São Paulo (USP)
(2)
Faculty of Pharmaceutical Sciences of Ribeirão Preto, USP
(3)
Faculty of Medicine of Ribeirão Preto, USP

Copyright

© Otaguiri et al; licensee BioMed Central Ltd. 2014

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. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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