Key result
EGCG-S treatment provided moderate protection against EV-69 cytotoxicity, with a maximum inhibition of infection of 47% in A549 cells at 75 µM and 24.5% in MRC-5 cells at 50 µM.
Why the study?
Pathogenesis of the recently identified enterovirus 69 (EV-69) is not well understood, and an antiviral with multiple mechanisms of action could help prevent enterovirus-mediated disease.
EGCG-S demonstrates moderate in vitro antiviral and antioxidant activity against Enterovirus 69 in human lung cells at concentrations below 100 μM.
EGCG-S shows no immediate clinical utility against EV-69; leaves open further preclinical optimization and in vivo testing.
Enteroviruses are responsible for emerging diseases which cause diverse symptoms and may result in neurological complications. An antiviral with multiple mechanisms of action can help prevent enterovirus mediated disease despite differences in the pathogenesis between enteroviruses, including the recently identified enterovirus 69 (EV-69) for which pathogenesis is not well understood. This study investigated the efficacy of epigallocatechin-3-gallate stearate (EGCG-S), a modified form of the antioxidant green tea catechin epigallocatechin-3-gallate (EGCG), in inhibiting EV-69 infection of lung fibroblast cells in vitro. Treatment with EGCG-S resulted in moderate protection from EV-69 mediated cytotoxicity as demonstrated by increased metabolic activity as well as maintenance of cell morphology and mitochondrial function. These effects were correlated with reduced hydrogen peroxide production in infected cells following EGCG-S treatment with concentrations less than 100 μM, suggesting a role for inhibition of EV-69 mediated oxidative stress. This study provides insight into characteristics of EV-69 infection as well as the efficacy of EGCG-S mediated inhibition of EV-69 infection.
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Mohamed et al. (2021) studied Enterovirus 69 infection (in vitro). EGCG-S (epigallocatechin-3-gallate stearate) vs. Untreated EV-69 infected cells was evaluated on Inhibition of EV-69 mediated cytotoxicity. EGCG-S treatment provided moderate protection against EV-69 cytotoxicity, with a maximum inhibition of infection of 47% in A549 cells at 75 µM and 24.5% in MRC-5 cells at 50 µM.
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