Transcriptome analysis following enterovirus 71 and coxsackievirus A16 infection in respiratory epithelial cells.
Jie Song, Yajie Hu, Weiyu Li, Hui Li, Huiwen Zheng, Yanli Chen, Shaozhong Dong, Longding Liu
Author Information
Jie Song: Yunnan Key Laboratory of Vaccine Research and Development on Severe Infectious Diseases, Institute of Medical Biology, Chinese Academy of Medical Science and Peking Union Medical College, Kunming, 650118, China.
Yajie Hu: Department of Respiratory Medicine, The First People's Hospital of Yunnan Province, Kunming, 650002, China.
Weiyu Li: Yunnan Key Laboratory of Vaccine Research and Development on Severe Infectious Diseases, Institute of Medical Biology, Chinese Academy of Medical Science and Peking Union Medical College, Kunming, 650118, China.
Hui Li: Yunnan Key Laboratory of Vaccine Research and Development on Severe Infectious Diseases, Institute of Medical Biology, Chinese Academy of Medical Science and Peking Union Medical College, Kunming, 650118, China.
Huiwen Zheng: Yunnan Key Laboratory of Vaccine Research and Development on Severe Infectious Diseases, Institute of Medical Biology, Chinese Academy of Medical Science and Peking Union Medical College, Kunming, 650118, China.
Yanli Chen: Yunnan Key Laboratory of Vaccine Research and Development on Severe Infectious Diseases, Institute of Medical Biology, Chinese Academy of Medical Science and Peking Union Medical College, Kunming, 650118, China.
Shaozhong Dong: Yunnan Key Laboratory of Vaccine Research and Development on Severe Infectious Diseases, Institute of Medical Biology, Chinese Academy of Medical Science and Peking Union Medical College, Kunming, 650118, China. dsz@imbcams.com.cn.
Longding Liu: Yunnan Key Laboratory of Vaccine Research and Development on Severe Infectious Diseases, Institute of Medical Biology, Chinese Academy of Medical Science and Peking Union Medical College, Kunming, 650118, China. longdingl@gmail.com. ORCID
Enterovirus 71 (EV-A71) and coxsackievirus A16 (CV-A16) are the major pathogens responsible for hand, foot and mouth disease (HFMD), but the mechanism by which these viruses cause disease remains unclear. In this study, we used transcriptome sequencing technology to investigate changes in the transcriptome profiles after infection with EV-A71 and CV-A16 in human bronchial epithelial (16HBE) cells. Using systematic bioinformatics analysis, we then searched for useful clues regarding the pathogenesis of HFMD. As a result, a total of 111 common differentially expressed genes were present in both EV-A71- and CV-A16-infected cells. A trend analysis of these 111 genes showed that 91 of them displayed the same trend in EV-A71 and CV-A16 infection, including 49 upregulated genes and 42 downregulated genes. These 91 genes were further used to conduct GO, pathway, and coexpression network analysis. It was discovered that enriched GO terms (such as histone acetylation and positive regulation of phosphorylation) and pathways (such as glycosylphosphatidylinositol (GPI)-anchor biosynthesis and DNA replication) might be closely associated with the pathogenic mechanism of these two viruses, and key genes (such as TBCK and GPC) might be involved in the progression of HFMD. Finally, we randomly selected 10 differentially expressed genes for qRT-PCR to validate the transcriptome sequencing data. The experimental qRT-PCR results were roughly in agreement with the results of transcriptome sequencing. Collectively, our results provide clues to the mechanism of pathogenesis of HFMD induced by EV-A71 and CV-A16.
References
Clin Transl Immunology. 2014 Oct 31;3(10):e28
[PMID: 25505956]
