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. 2022 Sep 15;13:985108. doi: 10.3389/fmicb.2022.985108

Figure 3.

Figure 3

The antiviral mechanism of Myricetin. (A) Mode of action study. Myricetin was added on PK-15 cells for 1 h, and after washing, the cells were infected with PRV (Pretreatment). Myricetin was incubated with PRV for 1 h, and then added into cells after dilution (Inactivation). Myricetin was mixed with PRV to infect cells and replaced by new culture medium after adsorbed 1 h at 4°C (Adsorption). Myricetin was added to cells after PRV adsorption for 1 h at 4°C, and then cells were incubated for 1 h at 37°C followed by wahsing with citric acid-sodium citrate buffer (Entry). Myricetin was added after cells was infected with PRV for 1 h at 37°C (Post-infection). (B) Time course of virucidal activity. PRV and myricetin were incubated for different time periods and then serially diluted on PK-15 cells for determining viral titers (TCID50). (C) Growth curve. After infection for 1 h, PK-15 cells were treated with myricetin and the viral gene copies at different time were detected. PRV, the infected group without treatment; PRV + Myr, the infected group with myricetin treatment (0.5 mM). Values are presented as means ± SD (n = 6). Symbols “** and ***” represent p < 0.01 and p < 0.001, respectively, between the PRV group and PRV + Myr group.