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Research Article Free access | 10.1172/JCI114341

Most CD4+ T cells from human immunodeficiency virus-1 infected patients can undergo prolonged clonal expansion.

E Langhoff, J McElrath, H J Bos, J Pruett, A Granelli-Piperno, Z A Cohn, and R M Steinman

Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

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Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

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Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

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Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

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Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

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Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

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Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

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Published November 1, 1989 - More info

Published in Volume 84, Issue 5 on November 1, 1989
J Clin Invest. 1989;84(5):1637–1643. https://doi.org/10.1172/JCI114341.
© 1989 The American Society for Clinical Investigation
Published November 1, 1989 - Version history
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Abstract

We have addressed the capacity of HIV-1 infection to alter the growth of primary CD4+ T cells, but at the clonal level. Single T cells were expanded in the presence of PHA, IL-2, and small numbers of accessory dendritic cells. We report two new findings. First, T cells from seropositive individuals, even those with AIDS and markedly reduced CD4+ counts, exhibit a normal cloning efficiency, and proliferative capacity. This result is in contrast to two prior reports of a low cloning efficiency in CD4+ T cells from HIV-1-infected patients. Second, when we added high doses of exogenous HIV-1 to T cell clones from control subjects, we observed infection but not cytotoxicity or loss of CD4+ cells, following addition of virus stocks at days 0, 3, and/or 7 of clonal growth. The same HIV-1 isolates markedly reduced CD4+ T cells in bulk mononuclear cultures. When tested at day 11, HIV-1 mRNA was expressed in some cells of exogenously infected clones by in situ hybridization; when tested at day 18, several clones could transactivate a TAT-sensitive cell line. These findings suggest that the loss of CD4+ T cells in infected individuals is not the inevitable result of the activation of latent infection, or spread of a productive infection, during clonal growth.

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