低致病性A/Anhui/1/2013(H7N9)流感病毒感染小鼠肺组织的miRNA表达谱分析.

[Objectives] This study aims to analyze host miRNAs in the regulation of influenza virus-host interaction using gene chip sequencing technology. [Methods] BALB/c mice were infected with low pathogenic A/Anhui/1/2013 (H7N9) virus and PBS. The lung tissues were collected at day 3 post-infection and were subjected to miRNA chip sequencing to screen differentially expressed miRNA and then verified by RT-qPCR. Targetscan, PITA and microRNAorg programs were used to predict target genes, respectively, and Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) were then used to analyze the biological functions of differential miRNA and their possible signaling pathways. [Resuts] Compared with the PBS infection group, 265 differentially expressed miRNA were detected in the low pathogenic H7N9 infection mice, of which 143 miRNA were significantly up-regulated and 122 miRNA were significantly down-regulated. The differentially expressed miRNA were verified by RT-qPCR, and the results of 10 candidates miRNA were consistent with the chip sequencing results. Further KEGG analysis indicated that these differentially expressed miRNA were mainly enriched in the Rap1 signaling pathway, PI3K-Akt signaling pathway, Hippo signaling pathway, MAPK signaling pathway, Wnt signaling pathway, focal adhesion, autophagy and other immune-related signaling pathways. Combined with differential mRNA information, miRNA-mRNA regulatory network revealed that there were mainly 15 differentially expressed miRNAs and 31 differential target genes enriched into these signaling pathways. [Conclusions] This experiment successfully screened differentially expressed miRNAs caused by low pathogenic H7N9 infection in mice lung tissue, and RT-qPCR proved that it had a good consistency with the expression trend of gene chip sequencing results. This study laid the foundation for further research of the important role of host miRNA in regulating influenza virus replication in mice model. [ABSTRACT FROM AUTHOR]