Abstract
We show here that HIV type 1 (HIV-1) Tat protein, in combination with anti-CD3/CD28 mAbs, promotes IL-2 production and proliferation of primary CD4(+) T lymphocytes, obtained from HIV-1-seronegative donors. This effect was observed when Tat was immobilized on a solid support, but it was not observed with soluble Tat. Such hyperactivation was accomplished by recruiting the rolipram-sensitive cyclic nucleoside phosphodiesterase 4 and resulted in increased susceptibility to HIV-1 infection. Accordingly, rolipram potently inhibited HIV-1 replication in cultures stimulated by anti-CD3/CD28 +/- Tat. These results add to the concept that decreasing Tat activity is an important addition to anti-HIV-1 therapy, and they suggest a target for anti-HIV-1 chemotherapy, phosphodiesterase 4.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3',5'-Cyclic-AMP Phosphodiesterases / antagonists & inhibitors
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3',5'-Cyclic-AMP Phosphodiesterases / metabolism
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3',5'-Cyclic-AMP Phosphodiesterases / physiology*
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CD4-Positive T-Lymphocytes / immunology*
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CD4-Positive T-Lymphocytes / metabolism
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CD4-Positive T-Lymphocytes / virology
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Cell Division / drug effects
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Cyclic AMP / metabolism
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Enzyme Inhibitors / pharmacology
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Gene Products, tat / metabolism*
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HIV-1 / drug effects
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HIV-1 / immunology*
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HIV-1 / physiology
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Humans
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Interleukin-2 / biosynthesis
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Intracellular Fluid / metabolism
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Lymphocyte Activation / immunology*
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Rolipram / pharmacology
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Virus Replication / immunology*
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tat Gene Products, Human Immunodeficiency Virus
Substances
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Enzyme Inhibitors
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Gene Products, tat
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Interleukin-2
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tat Gene Products, Human Immunodeficiency Virus
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Cyclic AMP
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3',5'-Cyclic-AMP Phosphodiesterases
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Rolipram