HIV type 1 persistence in CD4¯/CD8¯ double negative T cells from patients on antiretroviral therapy

Date

2006

Authors

Cheney, K.
Kumar, R.
Purins, A.
Mundy, L.
Fergusson, A.
Shaw, D.
Burrell, C.
Li, P.

Editors

Advisors

Journal Title

Journal ISSN

Volume Title

Type:

Journal article

Citation

AIDS Research and Human Retroviruses, 2006; 22(1):66-75

Statement of Responsibility

Kelly M. Cheney, Raman Kumar, Adrian Purins, Linda Mundy, Wendy Ferguson, David Shaw, Christopher J. Burrell, and Peng LI.

Conference Name

Abstract

The establishment of reservoirs of latently infected cells is thought to contribute to the persistence of HIV-1 infection in the host. Studies so far have mainly focused on the long-lived reservoir of HIV-infected resting CD4+ T cells. A discrete population of HIV-infected CD4¯/CD8¯ double negative (DN) T cells has recently been shown to exist and may also play a role in HIV-1 persistence. DN T cells are CD3 positive, either TCRαβ or TCRγδ positive, but lack both CD4 and CD8 surface markers. We developed a novel, magnetic bead column-based cell fractionation procedure for isolating >99% pure DN T cells. CD4+, CD8+, and DN T cells were purified from 23 samples of a cohort of 18 HIV-1-infected patients. Each cell fraction was analyzed for levels of total and integrated HIV-1 DNA. A correlation was observed between the presence of HIV-1 DNA in the DN T cell fraction and plasma viral load (VL). Using a micrococulture technique, we saw an initial release of virus from DN T cells of a patient with high VL. Analysis of env and nef sequence data suggested that the HIV-1 present in CD4+ and DN T cells originated from a common infecting strain. Different from the published literature, we have demonstrated the presence of HIV-1 DNA in DN T cells only in patients who are experiencing HAART failure. While these cells may have a limited role in viral persistence in high VL patients, our results suggest DN T cells are unlikely to be a major reservoir in patients on HAART with clinically undetectable plasma viral RNA.

School/Discipline

Dissertation Note

Provenance

Description

Access Status

Rights

© Mary Ann Liebert, Inc

License

Grant ID

Call number

Persistent link to this record