Volume 11 Supplement 1

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

Open Access

Role of regulatory proteins in HIV-1/HTLV-1 coinfection

  • Dustin Edwards1,
  • Klaus Strebel2,
  • Robyn Washington Parks1,
  • Cynthia Pise-Masison1,
  • Claudio Fenizia1,
  • Martina Fiocchi1 and
  • Genoveffa Franchini1Email author
Retrovirology201411(Suppl 1):P122

https://doi.org/10.1186/1742-4690-11-S1-P122

Published: 7 January 2014

In HTLV-1 endemic areas, 5 to 10% of HIV-1-infected individuals are also coinfected with HTLV-1/2. Several studies support the finding that dual infection of HIV-1 and HTLV-2 may confer delayed AIDS progression. In contrast, HTLV-1 has been concluded to have either no effect or to increase progression to AIDS in HIV-1-infected individuals. Although Tax-1 is known to influence HIV-1 replication in vitro, other HTLV-1 proteins likely have a role in retroviral coinfection. Here, we are investigating whether HTLV-1 proteins regulate activation of HIV-1 expression in latently-infected cells. In this study, we used B-cells infected with molecular clones that either express both p12 and p8, p12-only, p8-only, or contain knockouts to orf-I, orf-II, or hbz. The HTLV-1-infected B-cells were cocultured with KK1 T-cells latently-infected with HIV-1. Following coculture, cells and media were assayed for viral expression. Analyses of immunoblot and ELISA data suggest that HTLV-1-infected B-cells that express p8 enhanced activation of latent HIV-1 expression. We are currently examining whether cell-to-cell contact with p8 expressing cells is required to reactivate the latently-infected KK1 cells. Results from this study could have an impact on treatment of patients coinfected with HIV-1 and HTLV-1.

Authors’ Affiliations

(1)
Animal Models and Retroviral Vaccines Section, National Cancer Institute, National Institutes of Health
(2)
Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health

Copyright

© Edwards 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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