Genistein inhibits the replication of avian leucosis virus subgroup J in DF-1 cells

•Genistein inhibited viral gene expression and decreased the viral p27 protein level in DF-1 cells.•Genistein does not alert virus receptor expression and viral attachment.•Genistein does not interfere with virus entry, but significantly inhibited both viral gene transcriptions and virus release, wh...

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Veröffentlicht in:Virus research 2014-11, Vol.192, p.114-120
Hauptverfasser: Qian, Kun, Gao, Ai-jun, Zhu, Ming-yue, Shao, Hong-xia, Jin, Wen-jie, Ye, Jian-qiang, Qin, Ai-jian
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Sprache:eng
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Zusammenfassung:•Genistein inhibited viral gene expression and decreased the viral p27 protein level in DF-1 cells.•Genistein does not alert virus receptor expression and viral attachment.•Genistein does not interfere with virus entry, but significantly inhibited both viral gene transcriptions and virus release, which indicate that genistein exerts its inhibitory effects on the late phase of ALV-J replicative cycle.•Genistein effectively blocked ALV-J replication in DF-1 cells and may be useful for therapeutic drug design. To investigate the antiviral effects of genistein on the replication of avian leukosis virus subgroup J (ALV-J) in DF-1 cells, the cells were treated with genistein at different time points and the antiviral effects were examined by using a variety of assays. We determined that genistein strongly inhibited viral gene expression and decreased the viral protein level in the cell supernatant and the cytoplasm without alerting virus receptor expression and viral attachment. We also observed that genistein was not found to interfere with virus entry, but significantly inhibited both viral gene transcriptions at 24h post infection and virus release, which indicate that genistein exerts its inhibitory effects on the late phase of ALV-J replicative cycle. These results demonstrate that genistein effectively block ALV-J replication by inhibiting virus transcription and release in DF-1 cells, which may be useful for therapeutic drug design.
ISSN:0168-1702
1872-7492
DOI:10.1016/j.virusres.2014.08.016