Keeping in mind the diversity of clinical scenarios, we use the inclusive acronym ALI, one could think that it might be exactly this imprecise global view that prohibits the development of novel therapeutic approaches for ARDS. The diversity of underlying pathologic mechanisms prohibits the formulation of a unified pathophysiology of this clinical entity. Whether different forms of ALI (for example, direct versus indirect) are more of a response to a certain patho-mechanism than another remains to be determined. However, while there may be numerous diverse stimuli that can initiate the pathogenesis of this clinical entity, the final steps in ALI/ARDS, such as compromise of the alveolocapillary barrier function, appear to be somewhat common. Here we have reviewed the data which support the role of the activated PMN in lung injury as well as the contribution of epithelial cell death as independent entities contributing to ALI. Further, we have shown how recent studies looking at epithelial cells and the silencing of Fas-induced apoptosis and/or inflammation in these cells may serve as a lynchpin linking these two pathological processes. Upon early Fas activation, alveolar macrophages and lung epithelial cells might produce chemokines in the lung, thus attracting activated and potentially harmful neutrophils, monocytes, or even T-lymphocytes to the site of injury and potentiating the degree of injury. Finally, we trust we have illustrated how the application of siRNA-induced gene knockdown in the lung not only has produced novel insights into pathogenesis of ALI, but may represent a potential exciting therapeutic approach for its treatment. The cucumovirus 2b gene drives selection of inter-viral recombinants affecting the crossover site, the acceptor RNA and the rate of selection RNA–RNA recombination is an important pathway in virus evolution and has been described for many viruses. However, the factors driving recombination or promoting the selection of recombinants are still unclear. Here, we show that the small movement protein (2b) was able to promote selection of RNA 1/2–RNA 3 recombinants within a chimeric virus having RNAs 1 and 2 from cucumber mosaic virus, and RNA 3 from the related tomato aspermy virus, along with heterologous 2b genes. The source of the 2b also determined the selection of the acceptor RNA and the crossover site, as well as affecting the rate of selection of the recombinant RNAs. The nature of the RNA 3 also influenced the selection of the recombinant RNAs. A 163-nt tandem repeat in RNA 3 significantly affected the rate of selection of the recombinant RNA, while a single nucleotide within the repeat affected the crossover site. The recombination occurred in a non-random manner, involved no intermediates and probably was generated via a copy-choice mechanism during (+) strand RNA synthesis. RNA-RNA recombination is one of the most important pathways in virus evolution. It was first discovered in the early 1960s in poliovirus (1, 2) and has been documented in various genera of animal viruses, plant viruses and bacterial viruses group. Studies conducted on viruses during the last 40 years indicated that RNA-RNA recombination could occur between RNAs of the same or different strains of one species (3, 4) , of different species (5) or between viral and host cellular RNAs (6, 7) . RNA hairpins or mutations in a replicase domain have been implicated to play an important role in promoting RNA-RNA recombination (8) (9) (10) (11) . While none of those studies demonstrated a role for nonreplicase proteins in viral RNA-RNA recombination or selection of recombinants, recombination without replication has been described (12, 13) .