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. 2022 Aug 25;13:959577. doi: 10.3389/fmicb.2022.959577

Figure 3.

Figure 3

RK-33 decreases production of hCoV-OC43 and SARS-CoV-2. (A) RD cells were treated with various concentrations of RK-33 and cell viability determined post-treatment using CellTiter Glo assay. (B) RD cells were treated with RK-33 for 1 h followed by infection with hCoV-OC43 (MOI 0.1) and infectious titers at 3 dpi were determined via plaque assay. (C) RD cells were treated with RK-33 for 1 h followed by infection with hCoV-OC43 (MOI 0.1). CPE was observed at 4 dpi. (D) Calu-3 cells were treated with various concentrations of RK-33 and cell viability determined using CellTiter Glo assay. (E) Calu-3 cells were treated with various concentrations of RK-33 for 24 h followed by infection with SARS-CoV-2 Washington Variant (Lineage A; MOI 0.1) in the presence of RK-33. Cells were also post-treated with RK-33. Supernatants were collected at 48 hpi and plaque assays performed to determine infectious titers. DMSO was included as a negative control. (F) Calu-3 cells were treated with RK-33 (5 μM) or DMSO as described in panel E and viral titers determined by plaque assay. (G,H) Intra and extra cellular SARS-CoV-2 RNA viral copy numbers as measured by RT-qPCR of RdRp and E genes. Data represents the average of 3 biological replicates and error bars display standard deviations. *p < 0.05, **p < 0.005, ***p < 0.0005.