Figure 5

Impact of a deficiency in caspase-1/11, -3, or -7 or IL-1β/IL-18 in mice on rabies disease progression, mortality, brain viral load, and neutralizing antibody response upon infection with an attenuated strain of rabies. WT (n=6), caspase-1/11^−/− mice (n=6), caspase-3^−/− mice (n=4), caspase-7^−/− mice (n=5), and IL-1β/IL-18^−/− mice (n=4) were inoculated intranasally with the attenuated ERA virus (10⁵ TCID₅₀/mouse). Disease progression and mortality within each group was evaluated by mean clinical score per mouse (b) and survival curves (a), respectively. P-value was calculated using a log-rank test (survival curves) and an ANOVA test followed by Bonferroni multiple comparison post-test (mean score per mouse) and was indicated as follows: P-value <0.05 (*); P-value <0.01 (**). (a) All mice survived the infection except for one caspase-7^−/− mouse. (b) The mean clinical score per mouse was significantly different between WT and caspase-1^−/− inoculated with ERA virus at 21 and 20 DPI (c). Brain tissue was sampled at 35 DPI (except for one mouse) and viral load measured by RT-qPCR. P-value was calculated with an ANOVA test followed by Bonferroni multiple comparison post-test. No significant difference could be observed between WT mice and deficient mice. (d) The neutralizing antibody titer was evaluated by rapid fluorescent focus inhibition test and expressed in IU/ml. P-value was calculated by an ANOVA test followed by Bonferroni multiple comparison post-test. No significant difference was observed between WT and deficient mice, but antibody titers seemed higher in caspase-3^−/− mice.