However, even if these factors increased our estimated infection prevalence among proactively culled farms 5 fold (which seems unlikely from ongoing work), it would still mean that only a small proportion (,10%) of DCs and CPs culled were infected. This does not imply that proactive culling had no effect on the epidemic -as the largest expected effect of such culling is via the targeted depletion of susceptible animals. In this regard, proactive culling has the same epidemiological impact as vaccination. Future work will revisit past estimates of exactly how important such culling was for the control of the 2001 FMD epidemic. Efficient replication of pneumonia virus of mice (PVM) in a mouse macrophage cell line Pneumonia virus of mice (PVM; family Paramyxoviridae, subfamily Pneumovirinae) is a natural respiratory pathogen of rodent species and an important new model for the study of severe viral bronchiolitis and pneumonia. However, despite high virus titers typically detected in infected mouse lung tissue in vivo, cell lines used routinely for virus propagation in vitro are not highly susceptible to PVM infection. We have evaluated several rodent and primate cell lines for susceptibility to PVM infection, and detected highest virus titers from infection of the mouse monocyte-macrophage RAW 264.7 cell line. Additionally, virus replication in RAW 264.7 cells induces the synthesis and secretion of proinflammatory cytokines relevant to respiratory virus disease, including tumor necrosis factor-α (TNF-α), interferon-β (IFN-β), macrophage inflammatory proteins 1α and 1β (MIP-1α and MIP-1β) and the functional homolog of human IL-8, mouse macrophage inflammatory peptide-2 (MIP-2). Identification and characterization of a rodent cell line that supports the replication of PVM and induces the synthesis of disease-related proinflammatory mediators will facilitate studies of molecular mechanisms of viral pathogenesis that will complement and expand on findings from mouse model systems. Pneumonia virus of mice (PVM) infection in mice was originally described by Horsfall and colleagues [1, 2] , but until relatively recently, the sole interest in this virus was as a pathogen of laboratory rodent colonies [3] [4] [5] . Over the past several years, we and others have built on Horsfall's early studies, and have developed and characterized an in vivo model of severe respiratory virus infection using PVM [reviewed in [6, 7] ]. Among our findings, we have shown that a minimal, physiologically relevant inoculum of PVM (typically <100 pfu) results in robust virus replication in lung tissue, accompanied by influx of granulocytes in response to local production of specific proinflammatory chemokines [8] . The pathophysiology of PVM bronchiolitis leading to pneumonia and acute respiratory distress syndrome (ARDS) is similar to that observed in response to severe respiratory syncytial virus (hRSV) infection in human infants [9] .