Epigallocatechin-3-gallate rapidly remodels PAP85-120, SEM1(45-107), and SEM2(49-107) seminal amyloid fibrils

Castellano, Laura M.; Hammond, Rebecca M; Holmes, Veronica M.; Weissman, Drew; Shorter, James

doi:10.1242/bio.010215

Cited by 21 publications

(20 citation statements)

References 50 publications

(85 reference statements)

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“…In 2015, Castellano et al [36] investigated the anti-SEVI activity of EGCG ( 1 ) in greater detail. They confirmed that 1 can remodel all four classes of seminal amyloid, PAP248–286, PAP85–120, SEM1(45–107), and SEM2(49–107) at 200 μM and the viral infectivity was reduced to ~61%, ~35%, and 11% at 0.25 μM against the HIV-1 strain BL2, Bal, and 89.6, respectively.…”

Section: Antiviral Activity Of Catechins On Enveloped (−) Rna Virusmentioning

confidence: 99%

“…Regarding these biological properties, EGCG ( 1 ) has been reported to possess a broad spectrum of antiviral activities against DNA viruses such as herpes simplex virus (HSV; Herpesviridae ) [5,6,7,8,9,10,11], adenovirus ( Adenoviridae ) [10,12], human papilloma virus (HPV; Papovaviridae ) [13], and hepatitis B virus (HBV; Hepadnaviridae ) [14], and against (+)-RNA viruses such as hepatitis C virus (HCV; Flaviviridae ) [10,15,16,17,18,19], Zika virus (ZIKV; Flaviviridae ) [20,21,22,23], dengue virus (DENV; Flaviviridae ) [23,24], West Nile viruses (WNV; Flaviviridae ) [23], Chikungunya virus (CHIKV; Togaviridae ) [25], and Porcine Reproductive and Respiratory virus (PRRS; Atteriviridae ) [26], and (−)-RNA viruses such as human immunodeficiency virus (HIV; Retroviridae ) [27,28,29,30,31,32,33,34,35,36], Ebola virus (EBOV; Filoviridae ) [37] and influenza virus ( Orthomyxoviridae ) [2,10,38,39,40,41,42,43,44,45,46,47,48]. …”

Section: Introductionmentioning

confidence: 99%

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Antiviral Mechanism of Action of Epigallocatechin-3-O-gallate and Its Fatty Acid Esters

2018

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Epigallocatechin-3-O-gallate (EGCG) is the major catechin component of green tea (Cameria sinensis), and is known to possess antiviral activities against a wide range of DNA viruses and RNA viruses. However, few studies have examined chemical modifications of EGCG in terms of enhanced antiviral efficacy. This paper discusses which steps of virus infection EGCG interferes with, citing previous reports. EGCG appears most likely to inhibits the early stage of infections, such as attachment, entry, and membrane fusion, by interfering with viral membrane proteins. According to the relationships between structure and antiviral activity of catechin derivatives, the 3-galloyl and 5′-OH group of catechin derivatives appear critical to antiviral activities. Enhancing the binding affinity of EGCG to virus particles would thus be important to increase virucidal activity. We propose a newly developed EGCG-fatty acid derivative in which the fatty acid on the phenolic hydroxyl group would be expected to increase viral and cellular membrane permeability. EGCG-fatty acid monoesters showed improved antiviral activities against different types of viruses, probably due to their increased affinity for virus and cellular membranes. Our study promotes the application of EGCG-fatty acid derivatives for the prevention and treatment of viral infections.

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Section: Antiviral Activity Of Catechins On Enveloped (−) Rna Virusmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antiviral Mechanism of Action of Epigallocatechin-3-O-gallate and Its Fatty Acid Esters

2018

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“…As a polyphenolic compound found in green tea, EGCG has the ability to degrade the amyloid fibrils of human SEVI and block human SEVI-mediated HIV enhancement 6,39–41 . We showed here that EGCG could also degrade macaque SEVI-formed amyloid fibrils (Fig.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin Gallate Inhibits Macaque SEVI-Mediated Enhancement of SIV or SHIV Infection

Zhou

Guo

Liu

et al. 2017

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Background Human semen contains a factor that can enhance HIV infection up to 10^5-fold in cultures. This factor is termed SEVI (Semen-derived Enhancer of Virus Infection), which is composed of proteolytic fragments (PAP248-286) from prostatic acid phosphatase (PAP) in semen. Here, we examined whether macaque SEVI can facilitate simian immunodeficiency virus (SIV) or chimeric simian/human immunodeficiency virus (SHIV) infection. We also studied the effect of EGCG on macaque SEVI-mediated SIV or SHIV enhancement. Methods SIV or SHIV was mixed with different concentrations of macaque SEVI in the presence or absence of epigallocatechin gallate (EGCG). The mixture was added to cultures of TZM-bl cells or macaque PBMC. The effect of EGCG on macaque SEVI was measured by Congo-red staining assay, thioflavin T (ThT) fluorescence assay and visualized by a transmission electron microscope. Results We identified that there is one amino acid difference at the site of 277 between human PAP248-286 and macaque PAP248-286. Macaque SEVI significantly enhanced SIV or SHIV infection of TZM-bl cells and macaque PBMC. EGCG could block macaque SEVI-mediated enhancement of SIV or SHIV infection. Mechanistically, EGCG could degrade the formation of macaque SEVI amyloid fibrils that facilitates HIV attachment to the target cells. Conclusions The finding that macaque SEVI could enhance SIV or SHIV infection indicates the possibility to use the macaque SEVI in vivo studies with the macaque models. In addition, future studies are necessary to examine whether EGCG can be used as an effective microbicide for preventing SIV or SHIV mucosal transmission.

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“…An alternative strategy is to define ATP-independent protein disaggregases, which may couple binding energy to disaggregation and are operational outside cells. Select small molecules, including CLR01, a lysine- and arginine-specific molecular tweezer, and the green tea polyphenol, EGCG, can safely disaggregate or remodel diverse amyloids [57,58,59••,60]. A human Aβ oligomer- and fibril-specific monoclonal antibody, aducanumab, promotes clearance of Aβ plaques and may retard clinical decline in AD patients and is now in phase 3 trials [61••].…”

Section: Gene 3 Protein a Protein Disaggregase From Bacteriophage M13mentioning

confidence: 99%

Designer protein disaggregases to counter neurodegenerative disease

Shorter

2017

Current Opinion in Genetics & Development

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Protein misfolding and aggregation unify several devastating neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. There are no effective therapeutics for these disorders and none that target the reversal of the aberrant protein misfolding and aggregation that cause disease. Here, I showcase important advances to define, engineer, and apply protein disaggregases to mitigate deleterious protein misfolding and counter neurodegeneration. I focus on two exogenous protein disaggregases, Hsp104 from yeast and gene 3 protein from bacteriophages, as well as endogenous human protein disaggregases, including: (a) Hsp110, Hsp70, Hsp40, and small heat-shock proteins; (b) HtrA1; and (c) NMNAT2 and Hsp90. I suggest that protein-disaggregase modalities can be channeled to treat numerous fatal and presently incurable neurodegenerative diseases.

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Epigallocatechin-3-gallate rapidly remodels PAP85-120, SEM1(45-107), and SEM2(49-107) seminal amyloid fibrils

Cited by 21 publications

References 50 publications

Antiviral Mechanism of Action of Epigallocatechin-3-O-gallate and Its Fatty Acid Esters

Antiviral Mechanism of Action of Epigallocatechin-3-O-gallate and Its Fatty Acid Esters

Epigallocatechin Gallate Inhibits Macaque SEVI-Mediated Enhancement of SIV or SHIV Infection

Designer protein disaggregases to counter neurodegenerative disease

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