Volume 8 Supplement 1

15th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access

Tax-mediated re-routing of the HTLV-1 p13 protein to nuclear speckles

  • Vibeke Andresen1,
  • Cynthia A Pise-Masison1,
  • Uma Sinha-Datta2,
  • Robyn Washington Parks1,
  • Valentina Cecchinato1,
  • Risaku Fukumoto1,
  • Christophe Nicot2 and
  • Genoveffa Franchini1Email author
Retrovirology20118(Suppl 1):A125

https://doi.org/10.1186/1742-4690-8-S1-A125

Published: 6 June 2011

Human T-cell Leukemia Virus type-1 (HTLV-1) is highly immunogenic and has low variability so tight regulation of its expression is essential for virus maintenance in vivo. HTLV-1 replication is positively regulated by Tax and Rex, and negatively by the p30 and HBZ proteins. Here, we demonstrate that HTLV-1 encodes another negative regulator of virus expression, the p13 protein. Expressed separately, p13 localizes to the mitochondria, but in the presence of Tax, p13 is stabilized, and re-routed to the nuclear speckles. The p13 protein directly binds Tax, decreases Tax binding to the CBP/p300 transcriptional co-activator and, by reducing Tax transcriptional activity, suppresses viral expression. These findings suggest that HTLV-1 has evolved a complex mechanism to control its own replication through regulation of positive and negative viral proteins. Further, these results emphasize the importance of studying the function of the HTLV-1 viral proteins, not only in isolation, but also in the context of full viral replication.

Authors’ Affiliations

(1)
Animal Models and Retroviral Vaccines Section, National Cancer Institute
(2)
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center

Copyright

© Andresen 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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