Previous studies in which VSV vectors were delivered to mice intranasally showed that intranasal immunization with VSV induces the pro-inflammatory cytokine TNF-a, and that TNF-a production directly correlated with weight loss and acute pathology [14] . Although intranasal immunization has many advantages (needle free delivery, induction of mucosal immunity, etc), a significant drawback to intranasal immunization with rVSV is the risk of neurotropic spread of the virus. VSV instilled in the nose rapidly colonizes the olfactory neurons, and migrates into the brain [42] . The neurovirulence of VSV vectors has been significantly reduced by attenuating the capacity of the VSV vector to replicate [43] , but even a remote chance of neurotropic spread will likely prevent use of the intranasal route for human inoculations. Therefore, we decided to determine which cytokines were responsible for acute pathology after intramuscular immunization, which is regarded as a safer route by which to administer potentially neurotropic agents.