Respiratory syncytial virus (RSV) infection does not cause severe disease in most of us despite suffering from multiple RSV infections in our lives. However, infants, young children, older adults, and immunocompromised patients are unfortunately vulnerable to RSV-associated severe diseases. A recent study suggested that RSV infection causes cell expansion, resulting in bronchial wall thickening in vitro. Whether the virus-induced changes in the lung airway resemble epithelial-mesenchymal transition (EMT) is still unknown. Here, we report that RSV does not induce EMT in three different in vitro lung models: the epithelial A549 cell line, primary normal human bronchial epithelial cells, and pseudostratified airway epithelium. We found that RSV increases the cell surface area and perimeter in the infected airway epithelium, which is distinct from the effects of a potent EMT inducer, TGF-β1-driven cell elongation-indicative of cell motility. A genome-wide transcriptome analysis revealed that both RSV and TGF-β1 have distinct modulation patterns of the transcriptome, which suggests that RSV-induced changes are distinct from EMT.
Keywords: A549 cells; ALI culture; E-cadherin; NHBE cells; TGF-β; cytoskeleton; epithelial-mesenchymal transition (EMT); respiratory epithelium; respiratory syncytial virus (RSV); vimentin.