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. 2019 Aug 5;164(11):2659–2669. doi: 10.1007/s00705-019-04362-2

Fig. 4.

Fig. 4

poIRF1 restricts TGEV infection and plays an essential role in the IFN-γ-mediated inhibition of TGEV infection. (a, b) IRF1 knockdown abolishes IFN-γ-mediated inhibition of TGEV. ST cells were transfected with NC or shIRF1 s and then treated with 100 ng of IFN-γ per mL, followed by infection with TGEV. Cells were harvested at 24 h for quantification of the TGEV genome (a) and determination of the virus titer (b). (c, d) Knockdown of poIRF1 promotes TGEV replication without IFN-γ stimulation. ST cells were transfected with NC or shIRF1 s and subsequently infected with TGEV. After 24 h, cells were harvested for quantification of the TGEV genome (c) and determination of the virus titer (d). (e-g) Transient expression of IRF1 inhibits TGEV infection. ST cells were transfected with poIRF1-HA for 24 h and then infected with wild-type TGEV (e and f) or TGEV-GFP (g). TGEV infection was determined by measuring TGEV genomic RNA (e) and the viral titer (f). GFP-positive cells at 24 h after TGEV-GFP infection are shown (g). Data are shown as the mean ± SEM. Significance was determined by Student’s t-test compared to empty vector. *, p < 0.5; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001