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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/111702


    Title: Epigallocatechin-3-gallate inhibits the early stages of Japanese encephalitis virus infection
    Authors: Ching-Y, 6.;Wang, 6. Ching-Ying;黃素華;Huang, Su-Hua;林振文*
    Contributors: 生物科技學系
    Date: 2018-07
    Issue Date: 2018-12-25 10:55:35 (UTC+8)
    Abstract: Epigallocatechin-3-gallate (EGCG), a green tea catechin, shows broad sepectrum antiviral activity against many RNA and DNA viruses. This study investigated the antiviral efficacy of EGCG against Japanese encephalitis virus (JEV), a zoonotic flavivirus in Southeast Asia and the Western Pacific region. EGCG concentration-dependently reduced CPE, sub-G1 phase, and virus yield of infected cells with different JEV strains at different MOIs. The antiviral activity of EGCG against JEV in different assays declined in the following order: virus yield (IC50 of 7.0 μM) > virus attachment (IC50 of 7.9 μM) > virus entry (IC50 of 9.4 μM) > receptor binding and post-entry. However, EGCG had no virucidal effect on the infectivity of JEV particles. The results indicated that antiviral mechanism of EGCG against JEV was associated with blocking the early steps of JEV infection. The study suggests EGCG as a lead compound for developing broad-spectrum antiviral agents.
    Epigallocatechin-3-gallate (EGCG), a green tea catechin, shows broad sepectrum antiviral activity against many RNA and DNA viruses. This study investigated the antiviral efficacy of EGCG against Japanese encephalitis virus (JEV), a zoonotic flavivirus in Southeast Asia and the Western Pacific region. EGCG concentration-dependently reduced CPE, sub-G1 phase, and virus yield of infected cells with different JEV strains at different MOIs. The antiviral activity of EGCG against JEV in different assays declined in the following order: virus yield (IC50 of 7.0 μM) > virus attachment (IC50 of 7.9 μM) > virus entry (IC50 of 9.4 μM) > receptor binding and post-entry. However, EGCG had no virucidal effect on the infectivity of JEV particles. The results indicated that antiviral mechanism of EGCG against JEV was associated with blocking the early steps of JEV infection. The study suggests EGCG as a lead compound for developing broad-spectrum antiviral agents.
    Relation: VIRUS RESEARCH
    Appears in Collections:[Department of Biotechnology] Journal Article

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