Abstract
Amphotericin B derivatives, such as MS-8209, have been evaluated as a therapeutic approach to human immunodeficiency virus (HIV) infection. We show that MS-8209, like amphotericin B, increases tumor necrosis factor alpha (TNF-alpha) mRNA expression and TNF-alpha production and consequently HIV replication in human macrophages. These effects confirm the pharmacological risk associated with the administration of amphotericin B or its derivatives to HIV-infected patients.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amphotericin B / analogs & derivatives*
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Amphotericin B / pharmacology
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Anti-HIV Agents / pharmacology*
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HIV / drug effects*
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HIV / physiology
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Humans
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Macrophages / metabolism
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Macrophages / virology*
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RNA, Messenger / biosynthesis
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Risk Factors
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Tumor Necrosis Factor-alpha / biosynthesis*
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Tumor Necrosis Factor-alpha / drug effects
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Virus Replication / drug effects
Substances
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Anti-HIV Agents
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RNA, Messenger
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Tumor Necrosis Factor-alpha
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MS 8209
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Amphotericin B