Identification and characterization of circular RNAs in the A549 cells following Influenza A virus infection.

Influenza A virus (IAV) is one of the most dominant zoonotic-pathogen that causes annually recurring epidemic disease. The detailed molecular mechanism underlying IAV infection is still not fully understood. Circular RNAs (circRNAs) are generated from RNA back-splicing and involved in diverse biological processes. Here, we employed high-throughput circRNA microarray technology to profile circRNA expression in A549 cells in response to IAV infection. The analysis data revealed that 178 circRNAs expression were significantly upregulated while 137 downregulated, respectively, compared to the mock (P＜0.05, Fold Change＞2). Subsequently, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were also conducted. Moreover dysregulated circRNAs were characterized, and of which nine were verified by quantitative real-time PCR (qRT-PCR). We further confirmed that circRNA_0082633 expression was increased following IAV infection. Overexpression of circRNA_0082633 suppressed IAV infection while depletion of circRNA_0082633 promoted viral proliferation. Interestingly, the activation of Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling was involved in IAV-induced circ_0082633 expression. More importantly, we demonstrated that circ_0082633 expression enhanced type I interferon (IFN) signaling by IFN-stimulated response element (ISRE) promoter activity and Ifnb1 mRNA levels. These data firstly provided the expression profile of circRNAs in PR8-infected A549 cells and shed new light on the pathogenesis research of IAV infection. Our findings also suggest that circRNA_0082633 served an important function in IAV infection.