The second question arising from our results is how the VSVinduced production of IL-1 might be suppressed. One means of suppressing the biological response to IL-1 in humans is via injection of recombinant IL-1 receptor antagonists. Currently marketed as the drugs Anakinra or Kineret, these agents effect a systemic suppression of IL-1a and IL-1b. Although systemic suppression of IL-1 is an effective treatment for some conditions (severe rheumatoid arthritis, for example) [57] , systemic suppression of IL-1 also carries the risk of enhanced susceptibility to infection [57, 58] . Therefore we decided to determine whether there might be a way of suppressing IL-1 only in the cells directly infected with VSV, or within the focus of VSV-infected cells. To determine the appropriate target molecule(s) to effect local suppression of IL-1, it was necessary to determine the mechanism by which IL-1 was being produced in our model. Several years ago, Muruve et al reported that adenovirus activated human monocytes (THP-1 cells) to produce IL-1b in vitro, and that IL-1b production was dependent upon NLRP3 and caspase-1 [51] . In the supplement to that manuscript, the authors reported that infection of THP-1 cells with VSV did not induce IL-1b production, although detailed methods for that study were not provided. In contrast to that, two more recent studies reported that VSV-infected THP-1 cells do produce IL-1b in vitro. In the first study, Poeck et al found that VSV induced production of IL-1b was dependent upon caspase-1, but not upon NLRP3 [22] . In contrast to that, Rajan et al found VSV mediated induction of IL-1b from THP-1 cells to be dependent on NLRP3, and dependent on caspase-1 [52] . It is likely that the discrepancies in these reports were due to subtle differences in experimental procedures, but the different outcomes reported by each of these groups highlight the complexity of elucidating the precise mechanism(s) by which VSV may induce IL-1.