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EGCG and HIV Treatment
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Green Tea for HIV Treatment? - Herb Research Foundation
May 2009
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| | Copyright © 2008 Jing Tea Brisbane Australia | |
By Rob McCaleb
The green tea flavonoid EGCG has potential therapeutic value for treatment to for HIV-1 infection
EGCG binds to the CD4 molecule on T-cells according to research conducted in 2006. “We
havedemonstrated clear evidence of high affinity binding of EGCG to the CD4 molecule. EGCG
has
potential use as an adjunctive treatment in HIV-1infection.”
J Allergy Cli, Immunol Williamson ME McCormick TG, Nance CL, Shearer WT.
2006;118:1369-1374.
The green tea flavonoid EGCG has potential therapeutic value for treatment to for HIV-1 infection
EGCG binds to the CD4 molecule on T-cells according to research conducted in 2006. “We
havedemonstrated clear evidence of high affinity binding of EGCG to the CD4 molecule. EGCG
has
potential use as an adjunctive treatment in HIV-1infection.”
J Allergy Cli, Immunol Williamson ME McCormick TG, Nance CL, Shearer WT.
2006;118:1369-1374.
Epigallocatechin gallate (EGCG), the main polyphenol in green tea, binds to the T-cell
receptor, CD4: potential for HIV-1 therapy. (Recent Abstracts)(Brief article)
BACKGROUND: The green tea flavonoid, epigallocatechin gallate (EGCG),has been proposed
to have an anti-HIV-1 effect by preventing the binding of HIV-1 glycoprotein (gp) 120 to the CD4
molecule on T cells.OBJECTIVE: To demonstrate that EGCG binds to the CD4 molecule at the
gpl20 attachment site and inhibits gp120 binding at physiologically relevant levels, thus
establishing EGCG as a potential therapeutic treatment for HIV-1 infection. METHODS: Nuclear
magnetic resonance spectroscopy was used to examine the binding of EGCG and control,
(-)-catechin, to CD4-IgG2 (PRO 542). Gp120 binding to human CD4+ T cells was analyzed by
flow cytometry. RESULTS: Addition of CD4 to EGCG produced a linear decrease in nuclear
magnetic resonance signal intensity from EGCG but not from the control, (-)-catechin. In
saturation transfer difference experiments, addition of 5.8 micromol/L CD4 to 310 micromol/L
EGCG produced strong saturation at the aromatic rings of EGCG, but identical concentrations of
(-)-catechin produced much smaller effects, implying EGCG/CD4 binding strong enough to
reduce gp120/ CD4 binding substantially. Molecular modeling studies suggested
a binding site for EGCG in the D1 domain of CD4, the pocket that binds gpl20. Physiologically
relevant concentrations of EGCG (0.2 micromol/L) inhibited binding of gp120 to isolated human
CD4+ T cells. CONCLUSION: We have demonstrated clear evidence of high-affinity binding of
EGCG to the CD4 molecule with a Kd of approximately 10 nmol/L and inhibition of gpl20 binding
to human CD4+ T cells.
CLINICAL IMPLICATIONS: Epigallocatechin gallate has potential use as adjunctive therapy in
HIV-1 infection.
receptor, CD4: potential for HIV-1 therapy. (Recent Abstracts)(Brief article)
BACKGROUND: The green tea flavonoid, epigallocatechin gallate (EGCG),has been proposed
to have an anti-HIV-1 effect by preventing the binding of HIV-1 glycoprotein (gp) 120 to the CD4
molecule on T cells.OBJECTIVE: To demonstrate that EGCG binds to the CD4 molecule at the
gpl20 attachment site and inhibits gp120 binding at physiologically relevant levels, thus
establishing EGCG as a potential therapeutic treatment for HIV-1 infection. METHODS: Nuclear
magnetic resonance spectroscopy was used to examine the binding of EGCG and control,
(-)-catechin, to CD4-IgG2 (PRO 542). Gp120 binding to human CD4+ T cells was analyzed by
flow cytometry. RESULTS: Addition of CD4 to EGCG produced a linear decrease in nuclear
magnetic resonance signal intensity from EGCG but not from the control, (-)-catechin. In
saturation transfer difference experiments, addition of 5.8 micromol/L CD4 to 310 micromol/L
EGCG produced strong saturation at the aromatic rings of EGCG, but identical concentrations of
(-)-catechin produced much smaller effects, implying EGCG/CD4 binding strong enough to
reduce gp120/ CD4 binding substantially. Molecular modeling studies suggested
a binding site for EGCG in the D1 domain of CD4, the pocket that binds gpl20. Physiologically
relevant concentrations of EGCG (0.2 micromol/L) inhibited binding of gp120 to isolated human
CD4+ T cells. CONCLUSION: We have demonstrated clear evidence of high-affinity binding of
EGCG to the CD4 molecule with a Kd of approximately 10 nmol/L and inhibition of gpl20 binding
to human CD4+ T cells.
CLINICAL IMPLICATIONS: Epigallocatechin gallate has potential use as adjunctive therapy in
HIV-1 infection.
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