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In cell culture, A549 monolayer also faithfully exhibits various aspects of RSV infection and RSV-host interaction, including robust virus growth, formation of syncytia, activation of NF-kappa B (NF-κB), and elaboration of a battery of cytokines in response to virus infection [ 18 19 20 21 22 ] . In this paper we have, therefore, continued the use of A549 cells to elucidate the mechanism of RSV-actin interactions, and in particular, test the role of profilin in the pathways that are likely to involve such interactions.
The functionality of the RhoA of A549 cells is substantiated by a number of previous studies, such as the need for RhoA in bradykinin-mediated activation of NF-kappa B [ 35 ] , and the abrogation of H 2 O 2 -mediated activation of JNK by RhoA antisense oligonucleotide [ 36 ] . Profilin purified from A549 cells is also indistinguishable from HEp-2 cell profilin, in terms its molecular weight, pI, affinity for poly-proline, and ability to stimulate actin-dependent transcription of RSV genome in vitro [ 11 ] . Thus, the inability of A549 cells to elicit actin stress fibers is likely due to an as yet unidentified factor or pathway that may be altered or missing in the A549 cells.