Abstract
We report that the addition of an host paracaspase MALT1 inhibitor, MI-2, to HIV latently infected ACH-2, Jurkat E4, and J-LAT cells accelerated cell death in the presence of cell stimuli or the protein kinase C agonist, bryostatin 1. MI-2-mediated cell death correlated with the induction of the cellular RNase MCPIP1 and requires the presence of viral component(s). Altogether, the combination of MI-2 and bryostatin 1 displays selective killing of HIV latently infected CD4(+) T cells.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetanilides / pharmacology*
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Bryostatins / pharmacology*
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CD4-Positive T-Lymphocytes / drug effects*
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CD4-Positive T-Lymphocytes / virology
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Caspases / metabolism
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Cell Line, Tumor
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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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Humans
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Jurkat Cells
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Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein
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Neoplasm Proteins / antagonists & inhibitors*
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Neoplasm Proteins / metabolism
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Ribonucleases / metabolism
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Transcription Factors / metabolism
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Triazoles / pharmacology*
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Virus Activation / drug effects
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Virus Latency
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Virus Replication / drug effects
Substances
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Acetanilides
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Bryostatins
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MI-2 acetamide
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Neoplasm Proteins
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Transcription Factors
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Triazoles
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bryostatin 1
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Ribonucleases
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ZC3H12A protein, human
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Caspases
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MALT1 protein, human
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Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein