FIGURE 10.

Decreased inhibitory effect on type I IFN response stimulated by IFN-α/β in rD1 EV-A71-infected cells. (A) Induction of ISGs in rD1-infected cells. HeLa cells were infected with rFY or rD1 EV-A71 for 24 h, followed by treatment with or without IFN-α (25 ng/μL) for another 2 h. Total RNA was prepared from the cells for real-time RT-PCR to measure relative levels of the ISG gene transcripts. Values represented mean ± SD from triplicates of independent experiments. t tests were conducted on values from different groups. *P<0.05; **P<0.01; ***P<0.001. (B,C) Decreased reduction of ISGs and KPNA1 in rD1-infected cells. HeLa cells were infected with rFY or rD1 EV-A71 for 24 h, followed by treatment with or without IFN-α (B) or IFN-β (C) (25 ng/μL) for another 2 h. Cell lysates were prepared for western blot analyses with antibodies for MX1, OAS1, or KPNA1. (D) Increased translocation of p-STAT1/2 into the nucleus in rD1-infected cells. HeLa cells were infected with rFY or rD1 EV-A71 for 24 h, followed by stimulation with IFN-α (25 ng/μL) for another 30 min. The cytosolic and nuclear fractions were prepared from the cells for western blot analyses with antibodies for p-STAT1 or p-STAT2. β-tubulin and histone H3 were detected as loading controls for cytosolic and nuclear fractions, respectively.