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EGCG and HIV Treatment
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Inhibition of HIV-1 infectivity across subtypes by the green
tea catechin, epigallocatechin gallate (EGCG), without
altered immune function
tea catechin, epigallocatechin gallate (EGCG), without
altered immune function
June 2009
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Christina L Nance1, Edward B Siwak2, Melinda D'Souza1, Sonia Songa1, Ashley M McMullen1
and William T Shearer1
1 Pediatrics/Immunology 2 Molecular Virology and Microbiology, Baylor College of Medicine,
Houston, TX
and William T Shearer1
1 Pediatrics/Immunology 2 Molecular Virology and Microbiology, Baylor College of Medicine,
Houston, TX
Abstract
Previously, we presented evidence that the green tea catechin, epigallocatechin gallate (EGCG),
binds to the CD4 molecule at the gp120 attachment site on T cells. CD4+ T cells, B cells and
macrophages were isolated from HIV-1 uninfected donors. HIV-1 infectivity by HIV-1 p24 ELISA
on M-tropic (R5) subtypes B, C and G; T-tropic (X4) subtypes B and D; and dual tropic (R5/X4)
subtype B. Immune function studies: cytotoxicity by ViCell, apoptosis by flow cytometry,
immunoglobulin (Ig) production by ELISA and cytokine profiling by multiplex platform. Statistical
significance by Student's t test. EGCG significantly inhibited HIV-1 infectivity on human immune
cells in a dose-dependent manner (6-100µM) (p<0.01-0.001). At physiologic concentration of
6µM, EGCG significantly inhibited HIV-1 p24 antigen production across HIV-1 subtypes [B
(p<0.001), C, D, and G (p<0.01)]. The specificity of the EGCG-induced inhibition was
substantiated by the failure of EGCG derivatives lacking galloyl and/or pyrogallol side groups to
alter HIV-1 p24 levels. EGCG-induced inhibition of HIV-1 infectivity was not due to cytotoxcity, cell
growth inhibition, nor apoptosis. Neither Ig nor cytokine production were significantly altered.
EGCG inhibits HIV-1 infectivity across a broad spectrum of HIV-1 subtypes without significant
effects on immune function, thereby supporting EGCG as a candidate for HIV-1 therapy.
(NIH AT003084)
Previously, we presented evidence that the green tea catechin, epigallocatechin gallate (EGCG),
binds to the CD4 molecule at the gp120 attachment site on T cells. CD4+ T cells, B cells and
macrophages were isolated from HIV-1 uninfected donors. HIV-1 infectivity by HIV-1 p24 ELISA
on M-tropic (R5) subtypes B, C and G; T-tropic (X4) subtypes B and D; and dual tropic (R5/X4)
subtype B. Immune function studies: cytotoxicity by ViCell, apoptosis by flow cytometry,
immunoglobulin (Ig) production by ELISA and cytokine profiling by multiplex platform. Statistical
significance by Student's t test. EGCG significantly inhibited HIV-1 infectivity on human immune
cells in a dose-dependent manner (6-100µM) (p<0.01-0.001). At physiologic concentration of
6µM, EGCG significantly inhibited HIV-1 p24 antigen production across HIV-1 subtypes [B
(p<0.001), C, D, and G (p<0.01)]. The specificity of the EGCG-induced inhibition was
substantiated by the failure of EGCG derivatives lacking galloyl and/or pyrogallol side groups to
alter HIV-1 p24 levels. EGCG-induced inhibition of HIV-1 infectivity was not due to cytotoxcity, cell
growth inhibition, nor apoptosis. Neither Ig nor cytokine production were significantly altered.
EGCG inhibits HIV-1 infectivity across a broad spectrum of HIV-1 subtypes without significant
effects on immune function, thereby supporting EGCG as a candidate for HIV-1 therapy.
(NIH AT003084)
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