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. 2019 Apr 5;20(7):1695. doi: 10.3390/ijms20071695

Figure 2.

Figure 2

IFITs modulate CHIKV and ZIKV replication in HFF1 cells. (A) HFF1 cells were infected with CHIKV at a multiplicity of infection (MOI) of 1.0. At 24 and 48 hpi, infected cells were lysed with TETN-150 and analyzed by immunoblotting for the expression of IFIT1, IFIT2, IFIT3, MX1 and β-actin. (B) Similar to (A) but using ZIKV at a MOI of 1.0. For both (A,B), mock-infected cells were used as control. (C) CHIKV and (D) ZIKV RNA and infectious virus production were determined at 48 hpi in HFF1 cells transfected with an empty plasmid (pCtrl) or the same plasmid encoding IFIT proteins (pIFIT1, pIFIT2 and pIFIT3) by quantitative RT-PCR (black bars) and plaque assay (gray bars), respectively. The percentage of reduction as a function of the presence of each plasmid was calculated using the formula [1 − (R/C)] × 100, where C and R designate experimental values (RNA copy numbers or plaque numbers) in the presence of pCtrl and pIFIT, respectively. (E) CHIKV and (F) ZIKV RNA and infectious virus production were determined at 48 hpi in cells transfected with control siRNA (siCtrl) or siRNA, specific for IFIT (pIFIT1, pIFIT2 and pIFIT3) by real time RT-PCR (black bars) and plaque assay (gray bars), respectively. The data represent the mean values ± SD from three independent experiments. ** p < 0.01, as compared to siCtrl transfected cells.