Pre-treatment of cells (6 h before infection) with 2,000-kDa γ-PGA significantly increased its antiviral activity compared to post-infection treatment (1 h after infection) (Fig. 2c). This finding suggests that treatment with γ-PGA predisposes cells to acquire resistance to viral infection that is effective in suppressing MNV propagation. Additionally, the observation raised the possibility of γ-PGA interfering with the entry of MNV. Accordingly, a virus entry assay using Q-dot-conjugated norovirus was conducted. The result indicated the capability of γ-PGA to block the entry of norovirus into RAW264.7 cells (Fig. 2d,e) and explains a relatively lower antiviral activity in HG23 replicon cells than in MNV-infected macrophage cells.