Fig. 1
IFN-I signaling is an indispensable requirement in CNS neuroinflammation following distal JEV inoculation. a Essential role of IFN-I signaling in providing protection from JE. The susceptibility of C57BL/6 (BL/6) and IFNAR1 KO mice (n = 8–12) to JEV infection were monitored following different doses of viral inoculation (1 × 106, 5 × 106, 1 × 107, and 5 × 107 ffu/mouse) via intraperitoneal and footpad routes. The survival rate was examined over 15 days. b Viral burden in the non-lymphoid and lymphoid tissues at the periphery. Following JEV infection (5 × 106 ffu/mouse) via the footpad route, viral burden was assessed by real-time qRT-PCR at the indicated days pi in various tissues including popliteal LNs (pLNs), spleen, mesenteric LNs (mLNs), iliac LNs (iLN), bone marrow (BM), lung, liver, intestine, and kidney. c Viral burden in the CNS. Viral burden in the CNS tissues including spinal cord (SC) and brain was determined by real-time qRT-PCR using total RNA extracted from tissues. The viral RNA load was expressed by JEV RNA copy number per microgram of total RNA (n = 4). Each symbol represents the level in an individual mouse; the horizontal line indicates the mean ± SEM of each group. d Infectious JEV burden in both peripheral and CNS tissues. Following JEV infection (5 × 106 ffu/mouse) via the footpad route, the amount of infectious JEV was determined by a focus-forming assay using PBS-homogenates of the indicated tissues. Data in the graphs denote the mean ± SEM. Results are representative of one out of at least two individual experiments with four to five mice per group. Statistical significance *p < 0.05; **p < 0.01; ***p < 0.001 was assessed by an unpaired two-tailed Student’s t test