Abstract
Highly active antiretroviral therapy (HAART) can reduce plasma HIV-1 levels to below the detection limit. However, due to the latent reservoir in resting CD4(+) cells, HAART is not curative. Elimination of this reservoir is critical to curing HIV-1 infection. Agents that reactivate latent HIV-1 through nonspecific T cell activation are toxic. Here we demonstrate in a primary CD4(+) T cell model that the FDA-approved drug disulfiram reactivates latent HIV-1 without global T cell activation. The extent to which disulfiram reactivates latent HIV-1 in patient cells is unclear, but the drug alone or in combination may be useful in future eradication strategies.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, N.I.H., Intramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Anti-HIV Agents / therapeutic use
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CD4-Positive T-Lymphocytes / drug effects
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CD4-Positive T-Lymphocytes / virology*
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Cells, Cultured
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Disulfiram / pharmacology*
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Disulfiram / therapeutic use
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Genes, bcl-2
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HIV Infections / drug therapy
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HIV Infections / virology
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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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Lymphocyte Activation / drug effects*
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Transduction, Genetic
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Virus Activation / drug effects*
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Virus Latency / drug effects*
Substances
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Anti-HIV Agents
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Proto-Oncogene Proteins c-bcl-2
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Disulfiram