Fig. 4
Immunoglobulin can be detected in the brain of LACV-infected weanling mice but does not influence the development of neurological disease or neuropathology. a, b Detection of antibody in the brain by immunohistochemistry of LACV-infected weanling mice at the clinical time point (6 dpi) that were treated i.p. with Evans Blue dye 1 h prior to tissue removal. Brain tissue sections were analyzed for Evans Blue to detect vascular leakage (magenta) and either a rat Ig as a negative control or b mouse IgG (green) was used to detect leakage of antibodies into the brain. c Analysis of plasma from LACV-infected weanling mice at 4–5 dpi for NAb. Data are plotted as the limiting dilution for the inhibition of virus replication on a log2 scale. Each symbol represents an individual animal. d Weanling wildtype (n = 22), μMT -/- (n = 6), and Rag1 -/- (n = 10) mice develop neurological disease with similar rate and frequency. All mice were 3 weeks of age when infected i.p. with 103 PFU of LACV and followed for clinical disease. Statistical analysis was completed using the Mantel-Cox log-rank test with no significant difference detected. Representative, adjacent sections of brain tissue from e, g LACV-infected weanling wildtype and f, h Rag1 -/- mice with neurological disease (6–7 dpi) were stained for LACV (green) and active-Caspase 3 (white). Higher magnification insets in e and f show infected cells (LACV: green, DAPI: blue) with neuronal morphology within the hippocampus (red boxes). Insets in g and h demonstrate cells undergoing apoptosis (active-Caspase 3, white) within similar regions of the midbrain (red boxes) in both genotypes