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. 2013 Jun;87(11):6314–6325. doi: 10.1128/JVI.03213-12

Fig 1.

Fig 1

Induction of the IFN-α/β pathway and SG formation by picornavirus infection. (A and B) Immunofluorescence images of HeLa cells infected with coxsackievirus B3 (CVB3), mengovirus (mengo-wt), and mengovirus with a Zn-finger domain mutation in L (mengo-Zn) (MOI = 10). Cells were fixed at indicated time points and for G3BP (A) or dsRNA (B). Nuclei were stained using Hoechst-33258. (C) Immunofluorescence images of either mock-treated or mengo-Zn-infected (MOI = 10) HeLa cells. Cells were fixed 6 h.p.i. and stained using an antibody against TIA1. Nuclei were stained with Hoechst-33258. (D) Immunofluorescence images of mock-treated or mengo-Zn-infected (MOI = 10) MEF cells. Cells were stained using antibodies against G3BP (red) and SAM68 (green). Nuclei were stained with Hoechst-33258. TIA1 and G3BP form cytoplasmic aggregates upon mengo-Zn infection, while Sam68 maintains its nuclear localization. (E and F) In the same experiment as described for panel A, total RNA from infected cells was isolated and used for RT-qPCR analysis of intracellular viral RNA levels (E) and induction of IFN-β mRNA (F). Data are presented as the means ± standard deviations (SD) of the results of triplicate experiments.