Vitamin C and HIV
Vitamin C can inhibit the virus in test tubes, although it has not shown the same effect in the human body. It can help boost the immune system, however. Very high doses of vitamin C are sometimes used as supportive therapy. The dose must be determined and monitored by your doctor.
Ascorbate effect on cytokine stimulation of HIV production Harakeh S, Jariwalla RJ.Virology and Immunodeficiency Research Program, Linus Pauling Institute of Science and Medicine, Palo Alto, California 94306, USA Nutrition. 1995 Sep-Oct;11(5 Suppl):684-7
We have recently shown that ascorbic acid (AA) suppresses the production of HIV in a latently infected T-lymphocytic cell line (ACH-2) following stimulation with the tumor promoter, PMA. To evaluate the effect of ascorbic acid on virus activation following treatment with inflammatory cytokine, we tested tumor necrosis factor alpha (TNF-alpha) whose levels are elevated in patients with HIV/AIDS. ACH-2 cultures, pretreated with various nontoxic concentrations of ascorbate or AZT were stimulated for 2 h with TNF-alpha, and incubated further with fresh supplements of ascorbate or AZT. At 24 to 48 h post-treatment, the RT activity released into culture supernatant was determined. Results showed that TNF-alpha alone caused approximately 13- to 16-fold stimulation in the level of extracellular RT. Pretreatment with ascorbic acid at 200 micrograms/ml caused a little more than about 2- to 4-fold reduction in extracellular RT levels. Most remarkably, exposure to 300 micrograms/ml ascorbate resulted in approximately 5- to 10-fold lowering of the extra-cellular RT titer. In contrast, no significant suppression in extracellular RT levels was seen with concentrations of AZT in the range of 1-5 micrograms/ml.
NF-kappa B-independent suppression of HIV expression by ascorbic acid Harakeh S, Jariwalla RJ.Linus Pauling Institute of Science and Medicine, Palo Alto, California 94306, USA AIDS Res Hum Retroviruses. 1997 Feb 10;13(3):235-9
Ascorbic acid (ascorbate or vitamin C) has been shown to suppress the induction of HIV in latently infected T lymphocytic cells following stimulation with a tumor promoter (PMA) and inflammatory cytokine (TNF-alpha). To assess whether this inhibition was mediated via modulation of the cellular transcription factor, NF-kappa B, we carried out gel shift analysis on nuclear extracts prepared under different conditions of cell stimulation in the presence or absence of ascorbate, N-acetylcysteine (NAC), or zidovudine (AZT). Pretreatment of ACH-2 T cells by NAC followed by stimulation with PMA, TNF-alpha, or hydrogen peroxide (H2O2) resulted in strong suppression of NF-kappa B activation. In contrast, neither ascorbate nor AZT affected NF-kappa B activity under all three induction conditions in the ACH-2 cell line. Ascorbate and AZT also had no effect on NF-kappa B activation following TNF-alpha- or PMA-induced stimulation of U1 promonocytic cells. These results suggest that the molecular mechanism of HIV inhibition by ascorbate is not mediated via NF-kappa B inhibition, unlike that seen with other antioxidants.
Mechanistic aspects of ascorbate inhibition of human immunodeficiency virus Harakeh S, Niedzwiecki A, Jariwalla RJ.Viral Carcinogenesis and Immunology Program, Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306 Chem Biol Interact. 1994 Jun;91(2-3):207-15
We have investigated the molecular basis of the inhibitory effect of ascorbate (vitamin C) on human immunodeficiency virus (HIV) expression in unstimulated chronically infected and reporter cell lines. Comparison of intracellular HIV RNA and protein patterns of ascorbate-treated cells with corresponding patterns of untreated controls, did not show significant differences in the synthesis or processing of individual viral RNA and polypeptides, indicating that the inhibitory effect of ascorbate is not directed at steps of viral transcription or translation. Enzyme assays on cell extracts showed that the activity of an HIV LTR-directed reporter protein made in ascorbate-treated cells was reduced to approximately 11% relative to that of untreated control. These results, combined with previous observations on the suppression of HIV RT activity, are consistent with a mechanism of action in which ascorbate exerts a posttranslational inhibitory effect on HIV by causing impairment of enzymatic activity.
Comparative study of the anti-HIV activities of ascorbate and thiol-containing reducing agents in chronically HIV-infected cells Harakeh S, Jariwalla RJ.Viral Carcinogenesis Laboratory, Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306 Am J Clin Nutr. 1991 Dec;54(6 Suppl):1231S-1235S
To elucidate the action of vitamin C on pathogenic human retroviruses, we investigated and compared the effects of noncytoxic concentrations of ascorbic acid (AA), its calcium salt (Ca-ascorbate), and two thiol-based reducing agents [glutathione (GSH) and N-acetyl-L-cysteine (NAC)] against human immunodeficiency virus (HIV)-1 replication in chronically infected T lymphocytes. Ca-ascorbate reduced extracellular HIV reverse transcriptase (RT) activity by about the same magnitude as the equivalent dose of AA. Long-term experiments showed that continuous presence of ascorbate was necessary for HIV suppression. NAC (10 mmol/L) caused less than twofold inhibition of HIV RT and conferred a synergistic effect (approximately eightfold inhibition) when tested simultaneously with AA (0.426 mmol/L). In contrast, nonesterified GSH (less than or equal to 1.838 mmol/L) had no effect on RT concentrations and did not potentiate the anti-HIV effect of AA. These results further support the potent antiviral activity of ascorbate and suggest its therapeutic value in controlling HIV infection in combination with thiols.
Suppression of human immunodeficiency virus replication by ascorbate in chronically and acutely infected cells Harakeh S, Jariwalla RJ, Pauling L.Viral Carcinogenesis, Laboratory, Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306 Proc Natl Acad Sci U S A. 1990 Sep;87(18):7245-9
We have studied the action of ascorbate (vitamin C) on human immunodeficiency virus type 1 (HIV-1), the etiological agent clinically associated with AIDS. We report the suppression of virus production and cell fusion in HIV-infected T-lymphocytic cell lines grown in the presence of nontoxic concentrations of ascorbate. In chronically infected cells expressing HIV at peak levels, ascorbate reduced the levels of extracellular reverse transcriptase (RT) activity (by greater than 99%) and of p24 antigen (by 90%) in the culture supernatant. Under similar conditions, no detectable inhibitory effects on cell viability, host metabolic activity, and protein synthesis were observed. In freshly infected CD4+ cells, ascorbate inhibited the formation of giant-cell syncytia (by approximately 93%). Exposure of cell-free virus to ascorbate at 37 degrees C for 1 day had no effect on its RT activity or syncytium-forming ability. Prolonged exposure of virus (37 degrees C for 4 days) in the presence of ascorbate (100-150 micrograms/ml) resulted in the drop by a factor of 3-14 in RT activity as compared to a reduction by a factor of 25-172 in extracellular RT released from chronically infected cells. These results indicate that ascorbate mediates an anti-HIV effect by diminishing viral protein production in infected cells and RT stability in extracellular virions.
Sue :: Jan.11.2008 :: diet, pathology, research :: No Comments »