RESEARCH ARTICLE


Infection of CD8+CD45RO+ Memory T-Cells by HIV-1 and Their Proliferative Response



Naveed Gulzar1, 2, Sowyma Balasubramanian3, Greg Harris2, 3, Jaime Sanchez-Dardon3, Karen F.T. Copeland*
1 National HIV and Retrovirology Laboratories, Public Health Agency of Canada, Ottawa, Canada
2 Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Canada
3 Ottawa Health Research Institute, Ottawa, Canada


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Creative Commons License
© Gulzar et al.; Licensee Bentham Open

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

* National HIV and Retrovirology Laboratories, Public Health Agency of Canada, 200 Tunney’s Pasture Driveway Ottawa, Ontario, Canada K1A 0K9 Tel: 613-946-0365 Fax:613-948-4026 E-mail: karen_copeland@phac-aspc.gc.ca


Abstract

CD8+ T-cells are involved in controlling HIV-1 infection by eliminating infected cells and secreting soluble factors that inhibit viral replication. To investigate the mechanism and significance of infection of CD8+ T-cells by HIV-1 in vitro, we examined the susceptibility of these cells and their subsets to infection. CD8+ T-cells supported greater levels of replication with T-cell tropic strains of HIV-1, though viral production was lower than that observed in CD4+ T-cells. CD8+ T-cell infection was found to be productive through ELISA, RT-PCR and flow cytometric analyses. In addition, the CD8+CD45RO+ memory T-cell population supported higher levels of HIV-1 replication than CD8+CD45RA+ naïve T-cells. However, infection of CD8+CD45RO+ T-cells did not affect their proliferative response to the majority of mitogens tested. We conclude, with numerous lines of evidence detecting and measuring infection of CD8+ T-cells and their subsets, that this cellular target and potential reservoir may be central to HIV-1 pathogenesis.

Keyword: CD8+ T-Cell, HIV-1, memory, proliferation, subset.