Quantitative Proteomic Analysis of A549 Cells Infected with Human Respiratory Syncytial Virus

Munday, Diane C.; Emmott, Edward; Surtees, Rebecca; Lardeau, Charles-Hugues; Wu, Weining; Duprex, W. Paul; Dove, Brian K.; Barr, John N.; Hiscox, Julian A.

In HRSV infection, activation of retinoic acid-inducible gene-1 (RIG-I) induces an antiviral response (87) that involves its association with the mitochondrial antiviral signaling protein, allowing the recruitment of signaling adapters to the mitochondrial surface. Subsequent activation of the signaling complex is followed by translocation of NF-B into the nucleus and the activation of associated genes (88) . HRSV has been shown to activate cytoplasmic mitogen-and stressrelated kinase 1 (MSK1) via ROS, and in turn, MSK1 mediates NF-B activity (88) . Although the molecular basis for ROS-dependent MSK1 activation is unknown, the identification of pathways that control NF-B activation in response to HRSV infection may be useful in finding a way to attenuate the proinflammatory effects of HRSV and lung inflammation (88) . Bioinformatics analysis of quantitative proteomics data may highlight different pathways that lead to NF-B activation in HRSV-infected cells (e.g. Figs. 4 and 5) .