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Soluble Factors Secreted by Endothelial Cells Allow for Productive and Latent HIV-1 Infection in Resting CD4(+) T Cells.

Soluble Factors Secreted by Endothelial Cells Allow for Productive and Latent HIV-1 Infection in Resting CD4(+) T Cells.
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Morris JH, Nguyen T, Nwadike A, Geels ML, Kamp DL, Kim BR, Boyer JD, Shen A,


Morris JH, Nguyen T, Nwadike A, Geels ML, Kamp DL, Kim BR, Boyer JD, Shen A, (click to view)

Morris JH, Nguyen T, Nwadike A, Geels ML, Kamp DL, Kim BR, Boyer JD, Shen A,

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AIDS research and human retroviruses 2016 Oct 5()

Abstract

In vitro, it is difficult to infect resting CD4(+) T cells with human immunodeficiency virus type 1 (HIV), but infections readily occur in vivo. Endothelial cells (ECs) interact with resting CD4(+) T cells in vivo, and we found previously that EC stimulation leads to productive and latent HIV infection of resting CD4(+) T cells. In this study, we further characterize the interactions between EC and resting T cells. We found that resting CD4(+) T cells did not require direct contact with EC for productive and/or latent infection to occur, indicating the involvement of soluble factors. Among 30 cytokines tested in a multiplex enzyme-linked immunosorbent assay (ELISA), we found that expressions for IL-6, IL-8, and CCL2 were much higher in EC-stimulated resting T cells than resting T cells cultured alone. IL-6 was found to be the soluble factor responsible for inducing productive infection of resting T cells, although direct contact with EC had an added effect. However, none of the cytokines tested, IL-6, IL-8, or CCL2, induced additional latent infection in resting T cells, suggesting that unidentified cytokines were involved. Intracellular molecules MURR1, c-Jun N-terminal kinase (JNK), and glucose transporter-1 (GLUT1) were previously shown in blocking HIV infection of resting CD4(+) T cells. We found that the concentrations of these proteins were not significantly different in resting T cells before and after stimulation by EC; therefore, they are not likely involved in EC stimulation of resting CD4(+) T cells, and a new mechanism is yet to be identified.

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