Transcriptome analysis following EV-A71 and CV-A16 infection in respiratory epithelial cells
Background: Enterovirus 71 (EV-A71) and coxsackievirus A16 (CV-A16) are the major pathogens responsible for hand, foot and mouth disease (HFMD), but the detailed mechanism caused by the two viruses remains unclear. Methods: In this study, we aimed to adopt transcriptome sequencing technology to investigate changes in the transcriptome profiles after infection with EV-A71 and CV-A16 in human bronchial epithelial (16HBE) cells.
Results: Through 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 the EV-A71- and CV-A16-infected groups. A trend analysis of these 111 genes showed that there were 91 genes displaying the same trend in the EV-A71 and CV-A16 infection groups, including 49 upregulated genes and 42 downregulated genes. These 91 genes were further used to conduct GO, pathway, and coexpression network analyses. It was discovered that the 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 the 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.
Conclusions: Collectively, our results provide clues for the pathogenesis of HFMD induced by EV-A71 and CV-A16.
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Posted 13 Jan, 2020
Transcriptome analysis following EV-A71 and CV-A16 infection in respiratory epithelial cells
Posted 13 Jan, 2020
Background: Enterovirus 71 (EV-A71) and coxsackievirus A16 (CV-A16) are the major pathogens responsible for hand, foot and mouth disease (HFMD), but the detailed mechanism caused by the two viruses remains unclear. Methods: In this study, we aimed to adopt transcriptome sequencing technology to investigate changes in the transcriptome profiles after infection with EV-A71 and CV-A16 in human bronchial epithelial (16HBE) cells.
Results: Through 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 the EV-A71- and CV-A16-infected groups. A trend analysis of these 111 genes showed that there were 91 genes displaying the same trend in the EV-A71 and CV-A16 infection groups, including 49 upregulated genes and 42 downregulated genes. These 91 genes were further used to conduct GO, pathway, and coexpression network analyses. It was discovered that the 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 the 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.
Conclusions: Collectively, our results provide clues for the pathogenesis of HFMD induced by EV-A71 and CV-A16.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6