Minocycline attenuates HIV infection and reactivation by suppressing cellular activation in human CD4+ T cells
Journal
Journal of Infectious Diseases
Journal Volume
201
Journal Issue
8
Pages
1132-1140
Date Issued
2010
Author(s)
Abstract
Treatment of human immunodeficiency virus (HIV) infection with highly active antiretroviral therapy (HAART) is effective but can be associated with toxic effects and is expensive. Other options may be useful for long-term therapy. The immunomodulatory antibiotic minocycline could be an effective, low-cost adjunctive treat-ment to HAART. Minocycline mediated a dose-dependent decrease in single-cycle CXCR4-tropic HIV infection and decreased viral RNA after infection of CD4+ T cells with HIV NL4-3. Reactivation from latency was also decreased in a primary CD4+ T cell-derived model and in resting CD4+ T cells from HIV-infected patients. Minocycline treatment resulted in significant changes in activation marker expression and inhibited prolif-eration and cytokine secretion of CD4+ T cells in response to activation. This study demonstrates that min-ocycline reduces HIV replication and reactivation and decreases CD4+ T cell activation. The anti-HIV effects of minocycline are mediated by altering the cellular environment rather than directly targeting virus, placing minocycline in the class of anticellular anti-HIV drugs. ? 2010 by the Infectious Diseases Society of America. All rights reserved.
SDGs
Other Subjects
chemokine receptor CXCR4; minocycline; virus RNA; antiviral activity; article; attenuation; CD4+ T lymphocyte; concentration response; controlled study; cytokine release; drug effect; human; human cell; Human immunodeficiency virus infection; lymphocyte proliferation; priority journal; protein expression; T lymphocyte activation; virus latency; virus reactivation; virus replication; Anti-HIV Agents; CD4-Positive T-Lymphocytes; Cell Transformation, Viral; Cells, Cultured; Cytokines; DNA, Viral; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; HIV; HIV Infections; Humans; Lymphocyte Activation; Minocycline; Reverse Transcriptase Polymerase Chain Reaction; RNA, Viral; Viremia; Virus Latency
Type
journal article