Several groups have recently shown that macrophage inflammatory protein (MIP)-1α is released from RSVinfected cells in culture [7, 21] ; MIP-1α was also detected in upper and lower airway secretions from RSV-infected patients [7, 8] . Interestingly, of the three aforementioned chemokines, MIP-1α is the one that is most closely correlated with the presence of eosinophil degranulation products; this, together with data from our PVM model of pneumovirus infection [22] , has suggested to us that MIP-1α plays a pivotal role in eosinophil recruitment in response to primary pneumovirus infection. Interestingly, production of MIP-1α in cell culture requires active viral replication [8] , which suggests that this response may proceed by a mechanism that is completely distinct from that which elicits production of RANTES and IL-8. However, no reports to date have addressed the molecular mechanism that underlies the RSV-mediated MIP-1α response.