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Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Type I IFN signaling limits hemorrhage-like disease after infection with Japanese encephalitis virus through modulating a prerequisite infection of CD11b+Ly-6C+ monocytes

Fig. 8

IFN-I signal is required to attenuate JEV replication in hepatocytes, enterocytes, and neuron cells. Primary hepatocytes, enterocytes, and cortical neuron cells generated from IFN-I signal-competent and -incompetent mice were infected with JEV at the indicated MOI (0.01, 0.1, and 1.0). a The replication of JEV RNA genome in hepatocytes, enterocytes, and neuron cells. JEV replication was assessed by detecting viral RNA levels with real-time qRT-PCR at the indicated time points pi. Viral RNA levels were expressed by JEV RNA copy number per microgram of total RNA. b The production of infectious JEV in hepatocytes, enterocytes, and neuron cells. The levels of infectious JEV in culture media were determined by focus-forming assay following JEV infection (1.0 MOI). c and d Impaired induction of RIG-I-like receptors (RLRs), IRFs, and IFN-stimulated genes (ISGs) in IFN-I signal-deficient hepatocytes and neuron cells. The mRNA levels of the indicated genes were determined by real-time qRT-PCR using total RNA extracted from primary hepatocytes (c) and cortical neuron cells (d) 48 h following JEV infection with different doses (0.01, 0.1, and 1.0 MOI). Data in the graphs denote the mean ± SEM derived from quadruplicated wells. Results are representative of one out of at least two individual experiments. Statistical significance *p < 0.05; **p < 0.01; ***p < 0.001 was assessed by an unpaired two-tailed Student’s t test

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