Fig. 3

Effects of C–C chemokine receptor type 1 (CCR1) on JEV proliferation. (a) LncRNA-SUSAJ1 transcript levels following treatment with inhibitors for 48 h as determined by RT-PCR (n = 3 per group), *P < 0.05 and **P < 0.01 VS vehicle. (b) Whole-cell lysates were harvested from the treatment groups as indicated. Immunoblotting was performed to detect NS3 protein levels using β-actin as an internal control. (c) Effects of JEV transcript levels were determined by RT-PCR after transfected with ASO (lncRNA-SUSAJ1) and ASO (NC) (n = 3 per group), **P < 0.01 VS Mock (JEV⁺). (d) Time course of CCR1 messenger RNA (mRNA) levels after JEV infection (n = 3 per group), *P < 0.05 VS ASO 0 h. (e) Knockdown of CCR1 in PK-15 cells by short interfering RNAs (siRNAs). Cells were transfected with CCR1 siRNAs or scrambled siRNA (si-scr) (n = 3 per group), *P < 0.05 and **P < 0.01 VS si-scr. (f) LncRNA-SUSAJ1 transcript levels after transfection with CCR1 siRNA, as determined by RT-PCR (n = 3 per group), *P < 0.05 VS si-scr. (g) Whole-cell lysates were harvested from the treatment groups as indicated. Immunoblotting was performed to detect NS3 protein levels using β-actin as an internal control. (h) Effects of JEV transcript levels were determined by RT-PCR after transfected with si-CCR1 and si-scr (n = 3 per group), **P < 0.01 VS si-scr