The IL-1 receptor binds IL-1a and IL-1b. Therefore because IL-1R2/2 mice were protected from pathology, it was possible that IL-1a, IL-1b, or both cytokines contributed to VSVassociated pathology in vivo. IL-1b has been well characterized as a mediator of acute inflammatory responses in mice and humans, namely the induction of fever and cachexia, the acute phase response, and upregulation of other inflammatory mediators such as IL-6 in response to infectious or non-infectious stimuli [44, 45] , reviewed in [46] . IL-1b is more commonly associated with these pathologies than is IL-1a. For example, IL-1b deficient mice, but not IL-1a deficient mice, are protected from fever after injection of turpentine [16, 17] . Similarly, IL-1b, but not IL-1a, is the etiologic agent of hereditary periodic fever syndromes and other ''autoinflammatory'' diseases in humans [47, 48] . IL-1a is more commonly associated with ''sterile'' inflammation that accompanies apoptotic cell death [49] , and with the exception of adenovirus mediated inflammation [50] has not been associated with pathology arising from viral infection. For these reasons, we predict that IL-1b is the primary mediator of pathology in our system, but further experiments will be required to formally exclude a role for IL-1a.