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• W2036542307 abstract "HIV-1 infection ultimately results in impaired specific immune function by virtue of the initial binding of the HIV-1 virion envelope glycoprotein 120 (gp120) to the CD4 receptor in complex with a chemokine receptor on the T-cell surface.1Kwong P Wyatt R Robinson J Sweet RW Sodroski J Hendrickson WA Structure of an HIV gp120 envelope glycoprotein in complex with the CD4 receptor and a neutralizing human antibody.Nature. 1998; 393: 648-659Crossref PubMed Scopus (2455) Google Scholar Even though gp120 elicits virus-neutralizing antibodies, HIV-1 eludes the immune system and leads to the onset of AIDS. Ever since the discovery of the virus as the causative agent, there has been an intense effort to develop therapeutic methods to inhibit or prevent infection.2Wei X Decker JM Wang S Hui H Kappes JC Wu X et al.Antibody neutralization and escape by HIV-1.Nature. 2003; 42: 307-312Crossref Scopus (1935) Google Scholar, 3Chinen J Shearer WT Molecular virology and immunology of HIV infection.J Allergy Clin Immunol. 2002; 110: 189-198Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar, 4Sleasman JW Goodenow MM HIV-1 infection.J Allergy Clin Immunol. 2003; 111: S582-S592Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar Among the immune-based strategies designed to prevent the fateful initial binding event between HIV-1 virion and target cell are chemokine analogs, chemokine receptor inhibitors, anti—HIV-1 monoclonal antibodies, fusion proteins, and vaccines.5Chinen J Shearer WT Immune-based therapies for HIV infection.in: Shearer WT Hanson IC Medical management of AIDS in children. WB Saunders, Philadelphia2003: 139-154Google Scholar As reported by Kawai et al6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar in this issue, a unique candidate in the fight against AIDS has recently been investigated: green tea, one of the world's most frequently consumed beverages. Green tea has been reported to provide a cornucopia of beneficial health activities, such as the prevention of cancer and cardiovascular disease.7Nakachi K Matsuyama S Miyake S Suganuma M Imai K Preventive effects of drinking green tea on cancer and cardiovascular disease: epidemiological evidence for multiple targeting prevention.Biofactors. 2000; 134: 49-54Crossref Scopus (355) Google Scholar, 8NCI, DCPC Chemoprevention branch and agent development committee Clinical development plan: tea extracts, green tea polyphenols, epigallocatechin gallate.J Cell Biochem. 1996; 26: S236-S257Google Scholar There are specific components of green tea that have been shown to have antimicrobial activity.9Okubo S Hara Y Mori F Shimamura T Bactericidal and anti-toxin activities of catechin on enterohemorrhagic Escherichia coli.J Jpn Assoc Infect Dis. 1997; 72: 211-217Google Scholar Recently, investigators have found that the antiviral effects can be targeted at HIV-1 infection.7Nakachi K Matsuyama S Miyake S Suganuma M Imai K Preventive effects of drinking green tea on cancer and cardiovascular disease: epidemiological evidence for multiple targeting prevention.Biofactors. 2000; 134: 49-54Crossref Scopus (355) Google Scholar, 10Yamaguchi K Honda M Ikigai H Hara Y Shimamura T Inhibitory effects of (−)-epigallocatechin gallate on the life cycle of human immunodeficiency virus type 1 (HIV-1).Antiviral Res. 2002; 53: 19-34Crossref PubMed Scopus (185) Google Scholar, 11Nakane H Ono K Differential inhibition of HIV-reverse transcriptase and various DNA and RNA polymerases by some catechin derivatives.Nucleic Acids Research. 1989; 21: 115-116Google Scholar, 12Fassina G Buffa A Benelli R Varnier OE Noonan DM Albinai A Polyphenolic antioxidant (−)-epigallocatechin-3-gallate from green tea as a candidate anti-HIV agent.AIDS. 2002; 16: 939-941Crossref PubMed Scopus (126) Google Scholar Although the multiplicity of purported health benefit effects of green tea stretches the length of credibility, the molecular evidence of anti-HIV effects put forth by Kawai et al6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar warrants further scrutiny. Green tea is the nonoxidized, unfermented product of leaves from the evergreen plant Camellia sinensis. The active components of green tea are the polyphenolic catechins, which include the isomers (−)-epicatechin, (−)-epicatechin gallate, (−)-epigallocatechin, and (−)-epigallocatechin gallate (EGCG)13Zaveri N Synthesis of a 3,4,5-trimethoxybenzoyl ester analogue of epigallocatchin-3-gallate (EGCG): a potential route to the natural product green tea catechin, EGCG.Organic Letters. 2000; 3: 843-846Crossref Scopus (62) Google Scholar (Fig 1). EGCG accounts for approximately 50% of the total amount of catechins.10Yamaguchi K Honda M Ikigai H Hara Y Shimamura T Inhibitory effects of (−)-epigallocatechin gallate on the life cycle of human immunodeficiency virus type 1 (HIV-1).Antiviral Res. 2002; 53: 19-34Crossref PubMed Scopus (185) Google Scholar EGCG binds strongly to many biological molecules and affects a variety of enzyme activities and signal transduction pathways at micromolar or nanomolar levels.14Lee MJ Maliakal P Chen L Meng X Bondoc FY Prabhu S et al.Pharmacokinetics of tea catechins after ingestion of green tea and (−)-epigallocatechin-3-gallate by humans: formation of different metabolites and individual variability.Cancer Epi Bio Prev. 2002; 11: 1025-1032Google Scholar It is this specific component of green tea that is thought to be responsible for the vast array of presumed health benefits. Among the properties ascribed to EGCG are anti-tumorigenic, anti-inflammatory, antioxidative, antiproliferative, antibacterial, and antiviral effects.8NCI, DCPC Chemoprevention branch and agent development committee Clinical development plan: tea extracts, green tea polyphenols, epigallocatechin gallate.J Cell Biochem. 1996; 26: S236-S257Google Scholar, 10Yamaguchi K Honda M Ikigai H Hara Y Shimamura T Inhibitory effects of (−)-epigallocatechin gallate on the life cycle of human immunodeficiency virus type 1 (HIV-1).Antiviral Res. 2002; 53: 19-34Crossref PubMed Scopus (185) Google Scholar, 12Fassina G Buffa A Benelli R Varnier OE Noonan DM Albinai A Polyphenolic antioxidant (−)-epigallocatechin-3-gallate from green tea as a candidate anti-HIV agent.AIDS. 2002; 16: 939-941Crossref PubMed Scopus (126) Google Scholar Epidemiologic and preclinical studies have shown that drinking green tea is associated with a lower incidence of human cancer.8NCI, DCPC Chemoprevention branch and agent development committee Clinical development plan: tea extracts, green tea polyphenols, epigallocatechin gallate.J Cell Biochem. 1996; 26: S236-S257Google Scholar, 15Kohlmeier L Weterings KG Steck S Kok FJ Tea and cancer prevention: an evaluation of the epidemiologic literature.Nutr Cancer. 1997; 27: 1-13Crossref PubMed Scopus (189) Google Scholar This protective effect of green tea has been observed in pancreatic, colon, rectal, skin, breast, prostate, liver, and lung cancer.8NCI, DCPC Chemoprevention branch and agent development committee Clinical development plan: tea extracts, green tea polyphenols, epigallocatechin gallate.J Cell Biochem. 1996; 26: S236-S257Google Scholar, 15Kohlmeier L Weterings KG Steck S Kok FJ Tea and cancer prevention: an evaluation of the epidemiologic literature.Nutr Cancer. 1997; 27: 1-13Crossref PubMed Scopus (189) Google Scholar The major component of green tea, EGCG, has been shown to have tumor antimetastatic and antiangiogenic activities, as has been observed in its inhibition of adhesion of carcinoma cells16Maeda-Yamamoto M Kawahara H Tahara N Tsuji K Hara Y Isemura M Effects of tea polyphenols on the invasion and matrix metalloproteinases activities of human fibrosarcoma HT1080 cells.J Agric Food Chem. 1999; 47: 2350-2354Crossref PubMed Scopus (163) Google Scholar and significant prevention of growth of new blood vessels.17Sartippour M Shao Z Heber D Beatty P Zhang L Liu C et al.Green tea inhibits vascular endothelial growth factor (VEGF) induction in human breast cancer cells.J Nutr. 2002; 132: 2307-2311PubMed Google Scholar EGCG is thought to be the most potent chemopreventive component of the catechins, inasmuch as it possesses both pyrogallol and galloyl moieties13Zaveri N Synthesis of a 3,4,5-trimethoxybenzoyl ester analogue of epigallocatchin-3-gallate (EGCG): a potential route to the natural product green tea catechin, EGCG.Organic Letters. 2000; 3: 843-846Crossref Scopus (62) Google Scholar (Fig 1). In HIV-1 infection, it is EGCG that is responsible for the reported antiviral effects of green tea.6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar, 11Nakane H Ono K Differential inhibition of HIV-reverse transcriptase and various DNA and RNA polymerases by some catechin derivatives.Nucleic Acids Research. 1989; 21: 115-116Google Scholar, 12Fassina G Buffa A Benelli R Varnier OE Noonan DM Albinai A Polyphenolic antioxidant (−)-epigallocatechin-3-gallate from green tea as a candidate anti-HIV agent.AIDS. 2002; 16: 939-941Crossref PubMed Scopus (126) Google Scholar Several mechanisms for the antiviral effects of EGCG on HIV-1 have been proposed. EGCG inhibits HIV-1 replication in human PBMCs in vitro by inhibiting the biochemical activity of HIV-1 reverse transcriptase, the result being a subsequent decrease in HIV p24 antigen concentration.11Nakane H Ono K Differential inhibition of HIV-reverse transcriptase and various DNA and RNA polymerases by some catechin derivatives.Nucleic Acids Research. 1989; 21: 115-116Google Scholar Other studies show that EGCG interferes with HIV-1 viral infection by virion destruction and HIV-1 reverse transcriptase inhibition.12Fassina G Buffa A Benelli R Varnier OE Noonan DM Albinai A Polyphenolic antioxidant (−)-epigallocatechin-3-gallate from green tea as a candidate anti-HIV agent.AIDS. 2002; 16: 939-941Crossref PubMed Scopus (126) Google Scholar Finally, EGCG induces virion destruction in vitro by deformation of phospholipids via binding to the surface of the viral envelope.10Yamaguchi K Honda M Ikigai H Hara Y Shimamura T Inhibitory effects of (−)-epigallocatechin gallate on the life cycle of human immunodeficiency virus type 1 (HIV-1).Antiviral Res. 2002; 53: 19-34Crossref PubMed Scopus (185) Google Scholar Kawai et al6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar have reported yet another anti—HIV-1 effect of EGCG, one that prevents the attachment of the HIV-1 virion, gp120, to CD4 molecules on T-helper cells. The researchers found that in human CD4 T cells, EGCG (25-250 μmol/L) downregulated the cell surface expression of CD4 by binding to the CD4 molecule, presumably at a binding site recognized by gp120. Alternate explanations for this theory were ruled out by the demonstrated absence of (1) CD4 shedding from the cell surface, (2) loss of CD4 molecules, and (3) CD4 endocytosis. Kawai et al6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar also demonstrated that EGCG could antagonize gp120 binding as a ligand for CD4 and demonstrated that EGCG effectively interfered with gp120 binding to lymphocytes. Indeed, the most important of the anti—HIV-1 properties of EGCG might be its blocking effect on gp120 as a ligand for CD4, thus preventing the initial encounter of the HIV-1 virion with CD4 T cells. HIV-1 entry depends on the sequential interaction of the gp120 exterior envelope glycoprotein with the receptors on the cell, CD4, and members of the chemokine receptor family. Initial binding of the HIV-1 virions to cells involves the interaction of the viral envelope protein gp120 with CD4.1Kwong P Wyatt R Robinson J Sweet RW Sodroski J Hendrickson WA Structure of an HIV gp120 envelope glycoprotein in complex with the CD4 receptor and a neutralizing human antibody.Nature. 1998; 393: 648-659Crossref PubMed Scopus (2455) Google Scholar Recombinant soluble CD4 proteins bind to the HIV-1 envelope glycoprotein gp120 and inhibit viral infection.18Arthos J Deen KC Chaikin MA Fornwald JA Sathe G Sattentau QJ et al.Identification of the residues in human CD4 critical for the binding of HIV.Cell. 1989; 57: 469-481Abstract Full Text PDF PubMed Scopus (276) Google Scholar High-affinity binding to gp120 occurs at the D1 domain of CD4.18Arthos J Deen KC Chaikin MA Fornwald JA Sathe G Sattentau QJ et al.Identification of the residues in human CD4 critical for the binding of HIV.Cell. 1989; 57: 469-481Abstract Full Text PDF PubMed Scopus (276) Google Scholar The primary sites for HIV-1 interactions are on loops that protrude from the variable-like D1 domain in analogy with immunoglobulin complementarity-determining regions. The D2 domain is intimately associated with D1 but is variable-like.18Arthos J Deen KC Chaikin MA Fornwald JA Sathe G Sattentau QJ et al.Identification of the residues in human CD4 critical for the binding of HIV.Cell. 1989; 57: 469-481Abstract Full Text PDF PubMed Scopus (276) Google Scholar Broadly neutralizing antibodies recognize discontinuous conserved epitopes on gp120, the most abundant of which are directed against the CD4 binding site and block gp120-CD4 interaction.19Ho DD McKeating JA Li XL Moudgil T Daar ES Sun NC et al.Conformational epitope on gp120 important in CD4 binding and human immunodeficiency virus type 1 neutralization identified by a human monoclonal antibody.J Virol. 1991; 65: 489-493PubMed Google Scholar There might be a somewhat similar mechanism for the EGCG-induced disruption of the gp120-CD4 interaction, with the blocking ligand attaching to the CD4 molecule. The report by Kawai et al6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar left off at defining the specific molecular binding mechanism involved in the EGCG-induced HIV-1 inhibition. We propose that the binding of the EGCG compound to the CD4 molecule would specifically involve the D1 domain at the sites on the CD4 molecule that are most critical for binding to gp120. Mutational analysis of CD4 has implicated residues from a portion of the extracellular amino-terminal domain (D1) in gp120 binding.20Wu H Myszka DG Tendian SW Brouillette CG Sweet RW Chaiken IM et al.Kinetic and structural analysis of mutant CD4 receptors that are defective in HIV gp120 binding.Proc Natl Acad Sci U S A. 1996; 93: 15030-15035Crossref PubMed Scopus (57) Google Scholar In HIV-1 infection, interatomic contacts, including van der Waals contacts and hydrogen bonds, are made between 22 CD4 residues and 26 gp120 amino acid residues. These residues are distributed over 6 segments of gp120. On CD4, the residues span from 25 to 64. The most critical of these residues are Phe 43 and Arg 59, with Phe 43 at the center of the cluster of residues involved in binding. Sixty-three percent of all interatomic contacts come from one span (40-48) in C′C″ of CD4; Phe 43 alone accounts for 23% of the total.1Kwong P Wyatt R Robinson J Sweet RW Sodroski J Hendrickson WA Structure of an HIV gp120 envelope glycoprotein in complex with the CD4 receptor and a neutralizing human antibody.Nature. 1998; 393: 648-659Crossref PubMed Scopus (2455) Google Scholar, 20Wu H Myszka DG Tendian SW Brouillette CG Sweet RW Chaiken IM et al.Kinetic and structural analysis of mutant CD4 receptors that are defective in HIV gp120 binding.Proc Natl Acad Sci U S A. 1996; 93: 15030-15035Crossref PubMed Scopus (57) Google Scholar Therefore, these might be potential EGCG binding sites, as illustrated in Fig 2. We examined the structure of CD4 using protein data base:1CDJ20Wu H Myszka DG Tendian SW Brouillette CG Sweet RW Chaiken IM et al.Kinetic and structural analysis of mutant CD4 receptors that are defective in HIV gp120 binding.Proc Natl Acad Sci U S A. 1996; 93: 15030-15035Crossref PubMed Scopus (57) Google Scholar to model an electron density map at 3 Å, and we highlighted the regions of residues Phe 43 and Arg 59 (Fig 2). Because of the inherent flexibility of the EGCG molecule (due to the 4 key dihedral angles essentially covering the entire 360-degree range of rotational freedom) and the size of the molecule,21Charlton A Haslam E Williamson M Multiple conformations of the proline-rich protein/epigallocatechin gallate complex determined by time-averaged nuclear Overhauser effects.J Am Chem Soc. 2002; 124: 9899-9905Crossref PubMed Scopus (86) Google Scholar there is a wide range of possible conformations for docking into the region flanked by Phe 43 and Arg 59. Although we do not offer this model of EGCG-inhibition of HIV-1 gp120 binding to CD4 as fact, the conformational fit of critical binding sites is plausible. Additional studies to better define the nature and specificity of EGCG binding to the CD4 molecule are needed. A crucial aspect of translating the observed effects of EGCG to clinically relevant strategies, as pointed out by Kawai et al,6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar is the requirement to achieve physiologically relevant concentrations. Inasmuch as tea catechins have poor bioavailability, most of the ingested EGCG does not get into the blood, and a significant fraction is eliminated presystemically.22Chow H Cai Y Alberts DS Hakim I Dorr R Shahi F et al.Phase I pharmacokinetic study of tea polyphenols following single-dose administration of epigallocatehin gallate and polyphenon E.Cancer Epi Bio Prev. 2001; 10: 53-58Google Scholar At present, phase I clinical trials involving pharmacokinetic studies of EGCG have shown that only a small percentage of the orally administered catechin appeared in the blood. Drinking the equivalent of 2 cups of green tea resulted in the mean peak plasma EGCG level of 0.17 μmol/L after 1.5 hours, and only 4% to 8% of the ingested EGCG was excreted in urine.14Lee MJ Maliakal P Chen L Meng X Bondoc FY Prabhu S et al.Pharmacokinetics of tea catechins after ingestion of green tea and (−)-epigallocatechin-3-gallate by humans: formation of different metabolites and individual variability.Cancer Epi Bio Prev. 2002; 11: 1025-1032Google Scholar, 23Pisters KM Newman RA Coldman B Shin DM Khuri FR Hong WK et al.Phase 1 trial of oral green tea extract in adult patients with solid tumors.J Clin Oncol. 2001; 19: 1830-1838Crossref PubMed Scopus (205) Google Scholar Therefore, the development of a capsular alternative to green tea or EGCG itself would be beneficial, though even in this form a patient might not be able to achieve the EGCG levels of 25 to 250 μmol/L used in the current in vitro study.6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar This provocative investigation raises again the question of using natural products in the treatments of serious diseases. By no means should the findings of this study by Kawai et al6Kawai KN Tsuno N Kitayama J Okaji Y Yazawa K Asakage M et al.Epigallocatechin gallate, the main component of tea polyphenol, binds to CD4 and interferes with gp120 binding.J Allergy Clin Immunol. 2003; 112: 951-957Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar be seen as an endorsement of the consumption of green tea (gallons of it, presumably) to counter HIV-1 infection, or, worse, as an alternative therapy to the wonderful life-restoring antiretroviral agents that we now have. Whether green tea could serve as part of a combination therapy, along with other anti-HIV therapies, is an unanswered question thus far. The potential competitive binding properties of EGCG for the CD4 binding sites by gp120, while intriguing, might not translate to an HIV-1 preventative strategy. Nevertheless, it is not improbable that green tea or its extracts will be involved in the future treatment of HIV-1 infection. We thank Drs Wah Chiu, Matthew Dougherty, and Matthew Baker (Baylor College of Medicine) and Dr Michael Williamson (University of Sheffield, United Kingdom) for assistance with the assessment of the 3-dimensional binding of EGCG to the CD4 molecule." @default.
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• W2036542307 title "Is green tea good for HIV-1 infection?" @default.
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