in the blood of any infected animal. Those results demonstrated that IL-1 is not required for the control of VSV replication in vivo. As shown in Figure 3B , serum neutralizing antibody titers against VSV were not significantly different in IL-1R2/2 (n = 4 per group per timepoint) and wild type mice (n = 5 per group per timepoint) at any time after immunization. When we used an MHC Class I tetramer to measure CD8 T cell responses to an immunodominant H-2 K b -restricted epitope (N-RGYVYQGL-C) in the VSV N protein [24] , IL-1R2/2 mice had slightly fewer anti-VSV N specific CD8 T cells in the blood than did wild type animals ( Figure 3C ) at 14 and 28 days after immunization, although the difference was only statistically significant at 14 days after immunization (P = 0.03, Two-tailed T test). Finally, to determine whether these immune responses were sufficient to protect wild type and IL-1R2/2 mice from re-challenge with rVSV, we challenged all animals intranasally with 1610 8 PFU of rVSV at eight weeks after the primary infection. As shown in Figure 3D , pre-immune wild type and pre-immune IL-1R2/2 mice were fully protected from rechallenge, while naïve wild type animals (n = 7, open triangles, Figure 3D ), lost up to 20% of their pre-infection body weight. Two out of the seven naïve animals succumbed to infection. Together, these results indicated that IL-1 was not required either for the control of rVSV replication in vivo, or for the generation of protective anti-VSV immune responses. The results also supported the idea that suppressing the production of or response to IL-1b in response to rVSV vector administration would not render rVSV vectors unsafe or non-immunogenic.