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  • Open Access

APH-2 and Tax expression are correlated with a HTLV-2 proviral load but not with lymphocytosis

  • Estelle Douceron1, 2, 3,
  • Zhanna Kaidarova4,
  • Paola Miyazato5,
  • Masao Matsuoka5,
  • Edward L Murphy4 and
  • Renaud Mahieux1, 2, 3Email author
Retrovirology20118(Suppl 1):A184

https://doi.org/10.1186/1742-4690-8-S1-A184

Published: 6 June 2011

Keywords

Cell ProliferationBlood SampleInfectious DiseasemRNA LevelCancer Research

The recent discovery of HBZ, an antisense protein, encoded by HTLV-1 allowed a new way of understanding how HTLV-1 induces the development of adult T cell leukemia/lymphoma (ATLL). HBZ mRNA is expressed in all HTLV-1 patients tested regardless of their clinical status. Furthermore HBZ mRNA level is positively correlated to the HTLV-1 proviral load and it involved in infected T cell proliferation. The HTLV-2 homolog of HBZ, APH-2, also represses the viral transcription from the 5' LTR. We therefore quantified APH-2 and Tax mRNA levels as well as proviral load in a series of 51 blood samples obtained from the HTLV Outcomes Study (HOST) cohort. These samples were divided in low, intermediate and high proviral load (PVL) groups. We first show that APH-2 was expressed in most (94%) samples, while Tax was expressed mostly in the high PVL group. A positive correlation was observed between PVL and Tax and between PVL and APH-2. Although lymphocytosis is commonly observed among HTLV-2 carriers, we also demonstrate that APH2, contrary to HBZ does not promote cell proliferation in vitro. These results were confirmed in vivo since we did not observe a correlation between APH-2 level and the lymphocyte count. Our results therefore demonstrate that APH-2 is frequently expressed in vivo in HTLV-2 carriers. However, and contrary to HBZ, APH-2 does not promote cell proliferation.

Authors’ Affiliations

(1)
Equipe Oncogenèse Rétrovirale, INSERM-U758 Virologie Humaine, Lyon, France
(2)
Ecole Normale Supérieure de Lyon, Lyon, France
(3)
IFR 128 Biosciences Lyon-Gerland, Lyon, France
(4)
University of California San Francisco, Blood Systems Research Institute, San Francisco, USA
(5)
Laboratory of Virus Immunology, Institute for Virus Research, Kyoto University, Kyoto, Japan

Copyright

© Douceron 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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