Abstract
Long noncoding RNAs (lncRNAs) have been reported to participate in regulating many biological processes, including immune response to influenza A virus (IAV). However, the association between lncRNA expression profiles and influenza infection susceptibility has not been well elucidated. Here, we analyzed the expression profiles of lncRNAs, miRNAs, and mRNAs among IAV-infected adult rat (IAR), normal adult rat (AR), IAV-infected junior rat (IJR), and normal junior rat (JR) by RNA sequencing. Compared with differently expressed lncRNAs (DElncRNAs) between AR and IAR, 24 specific DElncRNAs were found between IJR and JR. Then, based on the fold changes and P value, the top 5 DElncRNAs, including 3 upregulated and 2 downregulated lncRNAs, were chosen to establish a ceRNA network for further disclosing their regulatory mechanisms. To visualize the differentially expressed genes in the ceRNA network, GO and KEGG pathway analysis was performed to further explore their roles in influenza infection of junior rats. The results showed that the downregulated DElncRNA-target genes were mostly enriched in the IL-17 signaling pathway. It indicated that the downregulated lncRNAs conferred the susceptibility of junior rats to IAV via mediating the IL-17 signaling pathway.
Highlights
Influenza is an infectious respiratory disease mainly caused by influenza viruses [1]
The results of hematoxylin and eosin staining clearly showed that compared with IAVuninfected (AR and junior rat (JR)) groups, the lung tissue sections of influenza A virus (IAV)-infected (IAR and infected junior rat (IJR)) groups had higher levels of leucocyte infiltration and platelet aggregation in the airway and perivascular spaces (Figure 1)
After RNA sequencing (RNA-seq), plentiful raw data were got from 4 samples (AR, infected adult rat (IAR), JR, and IJR)
Summary
Influenza is an infectious respiratory disease mainly caused by influenza viruses [1]. Approximately 870,000 children in preschool are annually hospitalized worldwide due to influenza [4]. Though infectious respiratory disease can occur in all ages, children are more susceptible to influenza infection and have more severe symptoms because of the imperfect immune system [5]. Compared with other age groups, rates of influenza infection are usually the highest in children, especially in children with underlying chronic medical conditions [6]. It is reported that host genetic factors play an important role on child susceptibility to influenza infection [7]. The molecular mechanisms underlying the influenza-associated genes and progression of influenza remain largely ambiguous
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