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Retrovirology

, 11:P118 | Cite as

The antisense protein of HTLV-2 positively modulates HIV-1 replication

  • Cynthia Torresilla
  • Sonia Do Carmo
  • Émilie Larocque
  • Estelle Douceron
  • Jean-Michel Mesnard
  • Renaud Mahieux
  • Benoit Barbeau
Open Access
Poster presentation

Keywords

Jurkat Cell Reporter Gene Expression NFAT Activation Antisense Protein 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Unlike HTLV-1, HTLV-2 does not induce leukemia and has been tentatively associated with an HTLV-1-associated myelopathy-like disorder. It has been reported that HTLV-2/HIV-1 co-infected patients progress less rapidly to AIDS than HIV-1-infected individuals. Tax2 has been suggested to mediate this protective state by inducing MIP-1α expression and blocking HIV-1 infection. As cells from HTLV-2-infected individuals mainly express Antisense Protein 2 (APH-2), our objective was to determine if this protein might also intervene in controlling HIV-1 replication in dually infected individuals. Using Jurkat cells, we first demonstrated that both APH-2 and HBZ, the HTLV-1 analogue, equally induced MIP-1α in unstimulated and stimulated Jurkat T cells. To assess if APH-2 might directly affect HIV-1 replication, a full length luciferase-expressing proviral DNA was tested in Jurkat cells. Surprisingly, upon co-transfection with an APH-2 expression vector, an increase in luciferase activity was observed, while HBZ expression rather led to reduced reporter gene expression. Western blot analyses and ELISA assay further indicated that HIV-1 p24 levels were more important in APH-2-expressing cells. To determine if APH-2 was directly modulating HIV-1 LTR activity, both NF-κB and NFAT were tested in stimulated Jurkat cells. Unexpectedly, HBZ and APH-2 inhibited NF-κB and NFAT activation, albeit at different extent. In addition, LTR activation was also inhibited by both antisense proteins although APH-2 had a more modest effect. Our results thus highlight the complex interplay between HTLV antisense transcript-encoded proteins and HIV-1 expression and further studies will be required to determine the potential impact of APH-2 in HTLV-2/HIV-1-infected individuals.

Copyright information

© Torresilla 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.

Authors and Affiliations

  • Cynthia Torresilla
    • 1
  • Sonia Do Carmo
    • 1
  • Émilie Larocque
    • 1
  • Estelle Douceron
    • 2
  • Jean-Michel Mesnard
    • 3
  • Renaud Mahieux
    • 2
  • Benoit Barbeau
    • 1
  1. 1.Département des sciences biologiques and Centre de recherche BioMedUniversité du Québec à MontréalMontréalCanada
  2. 2.Oncogenèse Rétrovirale, Ligue Nationale Contre Le Cancer, CIRI, INSERM U1111-CNRS UMR5308Université Lyon 1, Ecole Normale Supérieure de Lyon, LabEx ECOFECTLyonFrance
  3. 3.Université Montpellier 1Centre d’études d’agents Pathogènes et Biotechnologies pour la Santé, CNRS, UM5236MontpellierFrance

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