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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Zika virus infection of mature neurons from immunocompetent mice generates a disease-associated microglia and a tauopathy-like phenotype in link with a delayed interferon beta response

Fig. 1

Primary cultured neurons (PCNs) from immunocompetent mice display a weak capacity to stop ZIKV replication. PCNs and MEFs from B6 embryos were either non-infected (NI) or ZIKV-infected at a multiplicity of infection (MOI) of 5. a, b Immunofluorescence using an anti-NS2B antibody (red) shows the presence of the non-structural NS2B protein encoded by ZIKV in a MEFs and b PCNs 48 h p.i. with filamentous actin (F-act) visualized in MEFs using phalloidin (grey) and neuronal beta-tubulin III visualized in PCNs using the TUJ1 antibody (grey). c–e) PCNs, unable to stop viral replication, display a delayed IFNB expression and response as shown by the relative expression levels of c ZIKV RNA and RNAs coding for d IFNB and e ISGs analyzed by RT-qPCR with respect to Rplp0 used as reference gene. Symbols represent values obtained from n = 4 and 5 independent experiments for MEFs and PCNs respectively, with a minimum of two different times p.i. analyzed per experiment. Bars represent means. Significance between neurons and MEFs at the indicated times p.i. were assessed by two-way ANOVA and Sidak’s multiple comparison test. P-value < 0.0001 (****), < 0.001 (***), < 0.01 (**) and < 0.05 (*). Scale bars = 10 µm

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