- Poster presentation
- Open Access
Role of regulatory proteins in HIV-1/HTLV-1 coinfection
© Edwards et al; licensee BioMed Central Ltd. 2014
- Published: 7 January 2014
- Infectious Disease
- Cancer Research
- Regulatory Protein
- Molecular Clone
- Endemic Area
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.
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.