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Mary Alice Harbison, Sunyoung Kim, Jacqueline M. Gillis, Scott M. Hammer, Effect of the Calcium Channel Blocker Verapamil on Human Immunodeficiency Virus Type 1 Replication in Lymphoid Cells, The Journal of Infectious Diseases, Volume 164, Issue 1, July 1991, Pages 53–60, https://doi.org/10.1093/infdis/164.1.53
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Abstract
Cell signaling events are known to affect human immunodeficiency virus type 1(HIV-1) replication. Treatment of lymphoid CEM cells with the calcium channel blocker verapamil (25–75 µM) enhanced HIV-1 expression in acute, whole virus infection experiments, despite lowering intracellular calcium levels, ablating the acute rise in intracellular calcium normally seen with infection, and lengthening the doubling time of cell replication. Verapamil had no effecton cell surface CD4 expression. Transfection of CEM cells with plasmids containing the HIV-1 long terminal repeat linked to the chloramphenicol acetyltransferase reporter gene showed that verapamil enhanced expression of the HIV-1 long terminal repeat in a dose-dependent fashion. This effect was abolished by mutations in the binding sites for nuclear factor κ-B. Electrophoretic mobility shift assays confirmed that verapamil induced nuclear factor κ-B activity in CEM cells. Thus, verapamil, in high concentrations, can potentiate HIV-1 replication in lymphoid cells,and this effect may be mediated by induction of nuclear factor κ-B.
- calcium channel blockers
- signal transduction
- mutation
- plasmids
- calcium
- binding sites
- chloramphenicol o-acetyltransferase
- electrophoretic mobility shift assay
- genes, reporter
- hiv-1
- terminal repeat sequences
- transfection
- virus diseases
- infections
- verapamil
- calcium level result
- lymphoid cells
- doubling time