Abstract
BackgroundRespiratory syncytial virus (RSV) is the leading viral pathogen associated with bronchiolitis and lower respiratory tract disease in infants and young children worldwide. The respiratory epithelium is the primary initiator of pulmonary inflammation in RSV infections, which cause significant perturbations of global gene expression controlling multiple cellular processes. In this study, differential display reverse transcription polymerase chain reaction amplification was performed to examine mRNA expression in a human alveolar cell line (SPC-A1) infected with RSV.ResultsOf the 2,500 interpretable bands on denaturing polyacrylamide gels, 40 (1.6%) cDNA bands were differentially regulated by RSV, in which 28 (70%) appeared to be upregulated and another 12 (30%) appeared to be downregulated. Forty of the expressed sequence tags (EST) were isolated, and 20 matched homologs in GenBank. RSV infection upregulated the mRNA expression of chemokines CC and CXC and interfered with type α/β interferon-inducible gene expression by upregulation of MG11 and downregulation of G1P3.ConclusionRSV replication could induce widespread changes in gene expression including both positive and negative regulation and play a different role in the down-regulation of IFN-α and up-regulation of IFN-γ inducible gene expression, which suggests that RSV interferes with the innate antiviral response of epithelial cells by multiple mechanisms.
Highlights
Respiratory syncytial virus (RSV) is the leading viral pathogen associated with bronchiolitis and lower respiratory tract disease in infants and young children worldwide
We analyzed the early response of epithelium to RSV infection using differential display (DD) polymerase chain reaction (PCR) amplification of mRNA
RSV induced mRNA differential display in SPC-A1 cells To obtain the DD profile of SPC-1A cells in the presence or absence of RSV infection, total cellular RNA was extracted at 24 h after viral infection
Summary
Respiratory syncytial virus (RSV) is the leading viral pathogen associated with bronchiolitis and lower respiratory tract disease in infants and young children worldwide. The respiratory epithelium is the primary initiator of pulmonary inflammation in RSV infections, which cause significant perturbations of global gene expression controlling multiple cellular processes. One pathway to upregulate chemokine gene expression was identified by the activation of mitogen-activated protein kinase and nuclear factor κB during RSV infection [11,12]. The latter signaling cascade cluster includes chemokines, transcriptional regulators, intracellular proteins regulating translation and proteolysis, and secreted proteins [4,9,13], which influence the onset and severity of asthma. RSV infection appears to cause widespread changes in gene expression, and multiple mechanisms are involved in the host innate immune response. Forty DD expression sequence tags (ESTs) were analyzed, and two IFN-inducible genes, G1P3 and MG11, were examined during RSV infection
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