Fig. 4

Knockdown of FAM111A or RFC3 abolished the inhibitory effect of IRF2 overexpression on ZIKV replication. The experiments were divided into 8 groups of 2FTGH cells which were transfected with pEmpty, pIRF2, siNC, siFAM111A, siRFC3, pIRF2 + siNC, pIRF2 + siFAM111A orpIRF2 + siRFC3, respectively, for 24 h. All the cells were infected with ZIKV at MOI of 0.5 and the mRNA expression levels of FAM111A (a), IRF2 (b) and ZIKV (d) were measured by RT-qPCR at 24 h-post-infection. 2FTGH cells was transfected with pEmpty or pIRF2 plasmid before being infected with ZIKV (MOI = 0.5) for 24 h. The relative ZIKV production in 2FTGH cells between pEmpty and pIRF2 (P = 0.047, F = 9.2) were significantly different. The relative ZIKV production in 2FTGH cells between siNC and siFAM111A (P = 0.000, F = 93.2) or siRFC3 (P = 0.000, F = 123.6). The relative ZIKV production in 2FTGH cells between pIRF2 and siFAM111A (pIRF2*siFAM111A, P = 0.000, F = 44.5) or siRFC3 (pIRF2*siFAM111A, P = 0.002, F = 18) were significantly different. The IRF2 protein expression (c) was detected with western blots (t test, *P < 0.05; **P < 0.01)