Fig. 3: Evaluation of in vitro antiviral activity of Y180.
a–d VeroE6-TMPRSS2 cells were infected with SARS-CoV-2 at 0.01 MOI. Lysates were collected at 24 h.p.i. for the detection of viral titre with RT–qPCR (n = 4). Viral RNA-dependent RNA polymerase (RdRp) gene copies in VeroE6-TMPRSS2 infected with WT (a), B.1.1.7 (b), B.1.617.1 (c) and P.3 (d). e–h, Calu3 cells were infected with SARS-CoV-2 at 1 MOI. Lysates were collected at 24 h.p.i. for the detection of viral titre with RT–qPCR (n = 4). Viral RdRp gene copies in cells infected with WT (e), B.1.1.7 (f), B.1.617.1 (g) and P.3 (h). i–l, VeroE6-TMPRSS2 cells were infected with 50–70 PFU SARS-CoV-2 followed by Y180 addition at 2 h.p.i. and fixation at 48 h.p.i. (n = 3). Plaque formation was counted in cells infected with WT (i), B.1.1.7 (j), B.1.617.1 (k) and P.3 (l). Inhibition of plaque formation was normalized to vehicle controls. m–p, VeroE6-TMPRSS2 cells were infected with SARS-CoV-2 at 1 MOI. Cell viability was determined at 48 h.p.i. by measuring luciferase activity in cells (n = 4) infected with WT (m), B.1.1.7 (n), B.1.617.1 (o) and P.3 (p). Luciferase readings were normalized to mock-treated controls without virus infection. Data were obtained from three independent experiments. All data are shown as mean ± s.d. Statistical significance was assessed by one-way ANOVA compared with the vehicle control group; Student’s t-test compared with RDV treatment group. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; NS, not significant.
