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  • Meeting abstract
  • Open Access

Regulation of AP-1 activity by the HTLV-2 APH-2 protein

Retrovirology20118(Suppl 1):A161

https://doi.org/10.1186/1742-4690-8-S1-A161

Published: 6 June 2011

Keywords

  • Leucine Zipper
  • Mediate Activation
  • Viral Gene Expression
  • Spastic Paraparesis
  • Transcriptional Effect

In contrast to HTLV-1 which causes adult T-cell leukemia/lymphoma (ATL/ATLL) and HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), the role of HTLV-2 in human disease is less clearly defined but infection is associated with rare lympho-proliferative and neurological disorders. Transcription from the 3’ LTR of the HTLV-1 and HTLV-2 genomes governs the expression of two antisense regulatory proteins named HBZ (HTLV-1 basic leucine zipper) and APH-2 (antisense protein of HTLV-2), respectively. HBZ possesses a bZIP motif that facilitates its interaction with several cellular bZIP proteins including CREB2 and members of the AP-1 family such as c-Jun, JunB and JunD. These interactions inhibit Tax dependent LTR activation via CREB and AP-1 leading to the suggestion that HBZ counteracts the function of Tax 1 resulting in reduced viral gene expression and the enhancement of persistence in infected cells. Similarly, APH-2 inhibits Tax 2 mediated activation of the HTLV-2 LTR by interacting with CREB despite the absence of a bZIP motif. In the present study we investigated the transcriptional effects of APH-2 on the AP-1 pathway compared to HBZ. We clearly show that APH-2 stimulates basal AP-1-mediated transcription. In contrast to HBZ, we found that APH-2 enhances the ability of c-Jun to activate AP-1 activity. Co-immunoprecipitation assays demonstrate that APH-2 interacts with c-Jun in 293T cells. Furthermore as shown for HBZ, APH-2 down regulates Tax 2B mediated activation of AP-1 activity. These preliminary results suggest that HBZ and APH-2 may have distinct biological properties, which may contribute to the differential pathogenic potential of HTLV-1 and HTLV-2.

Authors’ Affiliations

(1)
Centre for Research in Infectious Diseases, School of Medicine and Medical Science, University College Dublin, Dublin, Ireland

Copyright

© Marban 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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