To determine the predicted protomer structure of HRV-QPM, DeepView/Swiss-Pdb Viewer v3.7, [58] were used to locate and individually thread HRV-QPM amino acid sequences into HRV reference structures. Of the five HRV strains with empirically determined structural data available, HRV-14 [14] and -16 [49] shared the highest sequence identities with HRV-QPM in the regions chosen. Proteins VP1 to VP3 were aligned and threaded through HRV-16 (1ayn1, 1ayn2, 1ayn3 respectively) and VP4 through HRV-14 (1na1). Models were submitted to the SWISS-MODEL server for final threading analysis. The resulting HRV-QPM protein data bank files (PDB) were then matched and structurally aligned to a template HRV protomer (HRV-16, 1AYN) . Other picornavirus reference PDB files used in this study: HRV-2 (1FBN), HRV-3 (1RHI), HRV-14 (4RHV), CV-A21 (1Z7S), E-11 (1H8T), PV-1 (1HXS) and CV-B3 (1COV). Structural matching, alignments, ribbon figures, capsid predictions and root mean square deviation (RMSD) data were produced using Chimera [55] . Epithelial Cell Apoptosis and Neutrophil Recruitment in Acute Lung Injury—A Unifying Hypothesis? What We Have Learned from Small Interfering RNAs In spite of protective ventilatory strategies, Acute Lung Injury (ALI) remains associated with high morbidity and mortality. One reason for the lack of therapeutic options might be that ALI is a co-morbid event associated with a diverse family of diseases and, thus, may be the result of distinct pathological processes. Among them, activated neutrophil- (PMN-) induced tissue injury and epithelial cell apoptosis mediated lung damage represent two potentially important candidate pathomechanisms that have been put forward. Several approaches have been undertaken to test these hypotheses, with substantial success in the treatment of experimental forms of ALI. With this in mind, we will summarize these two current hypotheses of ALI briefly, emphasizing the role of apoptosis in regulating PMN and/or lung epithelial cell responses. In addition, the contribution that Fas-mediated inflammation may play as a potential biological link between lung cell apoptosis and PMN recruitment will be considered, as well as the in vivo application of small interfering RNA (siRNA) as a novel approach to the inhibition of ALI and its therapeutic implications. The aim of this review is, therefore, to elucidate mechanisms of ALI pathogenesis, focusing on two main theories. The first, that neutrophils (PMN) can play a central role in driving ALI and the second, that lung epithelial cell apoptosis represents an important pathological aspect inducing lung injury. In this regard, we discuss the data in the field as well as some of our own findings using a clinically relevant double-hit mouse model of indirect ALI induced by hemorrhagic shock and subsequent polymicrobial sepsis. In addition, a novel strategy, i.e. the use of siRNA in mouse lungs in vivo, has served us in broadening our understanding of the pathology of ALI.