Micronutrient Cooperation in Suppression of HIV Production in Chronically and Latently Infected Cells

R.J. Jariwalla, B. Gangapurkar, A. Pandit, T. Kalinovsky, A. Niedzwiecki, M. Rath
Molecular Medicine Reports 2010, 3:377-385

Abstract:
Nutrients are known to display pharmacologic activity against viruses and to exert cooperative effects in cells. To study the influence of nutrient cooperation on HIV production in chronically infected T lymphocytes, we evaluated the individual and combined effects of nutrients on HIV-1 reverse transcriptase (RT) released into the culture supernatant. In unstimulated cells, low concentrations of single nutrients namely, ascorbic acid (AA), green tea polyphenols (GT), or lysine did not significantly suppress HIV-1 RT production. However, when GT (25 μg/ml) and AA (32 μg/ml to 64 μg/ml) were combined and applied to cells, extracellular RT was significantly reduced relative to control. Combining GT (25 μg/ml) with lysine (25 μg/ml), also reduced RT level to a greater extent (51% of control) than that observed with lysine alone, and addition of AA (16 μg/ml) to the same combination decreased RT further to 17% of control (p=0.06).

Under the same assay conditions, the nucleoside analogue AZT did not significantly suppress HIV production at low to moderate concentrations (0.5 – 1.0 μg/ml) but reduced RT to 40% of control (p=0.02) at the highest dose tested (2 μg/ml). In both unstimulated and latently infected cells stimulated with mitogen (PMA or TNF-alpha), a nutrient mixture containing GT, AA and amino acids, gave significantly greater RT suppression than equivalent concentrations of key individual components. Nutrient effects on RT suppression were virus specific and not due to non-specific cellular toxicity. These results suggest that relatively nontoxic micronutrient combinations are more potent than single nutrients in suppressing virus production in chronically infected T cells, indicating cooperative effects of constituent nutrients in HIV inhibition.

Full Study:

Printable PDF