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Virol J. 2008; 5: 114.
Published online 2008 October 6. doi: 10.1186/1743-422X-5-114.
PMCID: PMC2572611
Inhibition of G1P3 expression found in the differential display study on respiratory syncytial virus infection
Dongchi Zhao,corresponding author1,2 Dan Peng,1 Lei Li,2 Qiwei Zhang,2 and Chuyu Zhang2
1Pediatrics Department, Zhongnan Hospital of Wuhan University Medical School, Donghu Road 169, Wuhan 430071, PR China
2Virology Institute, College of Life Science, Wuhan University, Wuhan 430072, PR China
corresponding authorCorresponding author.
Dongchi Zhao: zhaodong/at/public.wh.hb.cn; Dan Peng: pengdan83/at/hotmail.com; Lei Li: avlab/at/whu.edu.cn; Qiwei Zhang: avlab/at/whu.edu.cn; Chuyu Zhang: avlab/at/whu.edu.cn
Received August 17, 2008; Accepted October 6, 2008.
Abstract

Background
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. 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.

Results
Of 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.

Conclusion
RSV 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.