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Enhancement of human immunodeficiency virus 1 replication in monocytes by 1,25-dihydroxycholecalciferol
P R Skolnik1, B Jahn, M Z Wang
1Department of Medicine, Tufts University School of Medicine, Boston, MA.
Insights
Vitamin D (1,25-dihydroxycholecalciferol) significantly boosts human immunodeficiency virus type 1 (HIV-1) replication. This finding suggests vitamin D may be a potent factor influencing HIV-1 replication and potential therapeutic targets.
Area of Science:
- Virology
- Immunology
- Endocrinology
Background:
- Human immunodeficiency virus (HIV) replication is tightly regulated.
- Understanding factors that modulate HIV replication is crucial for therapeutic development.
Purpose of the Study:
- To investigate the effect of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] on HIV-1 replication.
- To explore the role of the 1,25-(OH)2D3 intracellular receptor in HIV-1 regulation.
Main Methods:
- Assessing HIV-1 replication in various cell types (monocyte cell lines, peripheral blood monocytes, PBMCs) with and without 1,25-(OH)2D3 treatment.
- Evaluating the impact of 1,25-(OH)2D3 precursors on HIV-1 replication.
Main Results:
- 1,25-(OH)2D3 enhanced HIV-1 replication by up to 10,000-fold.
- The degree of enhancement correlated with the affinity of 1,25-(OH)2D3 precursors for their intracellular receptor.
- HIV-1 replication was modulated in monocyte cell lines, peripheral blood monocytes, and unfractionated peripheral blood mononuclear cells.
Conclusions:
- 1,25-(OH)2D3 is a potent regulator of HIV-1 replication.
- The mechanisms likely involve the 1,25-(OH)2D3 intracellular receptor.
- These findings have implications for designing novel HIV-1 therapies.
Abstract:
Human immunodeficiency virus (HIV) expression and replication are under tight regulatory control. We demonstrate that 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] enhances the replication of monocyte- and lymphocyte-tropic strains of HIV-1 up to 10,000-fold in monocyte cell lines, peripheral blood monocytes, and unfractionated peripheral blood mononuclear cells. 1,25(OH)2D3 is therefore one of the most potent regulators of HIV-1 replication described to date. Precursors of 1,25(OH)2D3 enhance HIV-1 replication in proportion to their affinity for the 1,25(OH)2D3 intracellular receptor, suggesting that 1,25(OH)2D3 influences HIV-1 replication by mechanisms involving this receptor. These studies may have important implications for the design of effective therapy of HIV-1 infection.