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Identification of lncRNA-up4 as an Enhancer of Influenza A Virus Replication through Negatively Regulating the Innate Immune Response

ABSTRACT: Inflammation cause a critical role against immune response and activate the macrophages. Current studies have reported that long non coding RNAs (lncRNAs) regulate the gene expression by interacting with various biological molecules. Experimental research has provided insights into the functions of lncRNAs that have significant impact on host-virus dynamics, including response to IAV infections such as H9N2, WSN, and PR8.Given the global health threat posed by influenza A virus (IAV) and its association with severe pneumonia, we investigated the role of host lncRNAs in IAV infection and pathogenesis. RNA microarray analysis of chicken DF1 cells showed regulation changes in 2,118 lncRNAs following 12 hours of IAV infection (H9N2-VS-CON P-value<0.05 & |log2FC| >1). Notably, lncRNA-up4 exhibited significant up regulation post-IAV induction and was associated with IL-6, a critical cytokine involved in excessive inflammatory response to IAV. Functional analysis of lncRNA-up4 revealed that its depletion resulted in decreased viral NP protein accumulation and reduced IL-6, TNFα, IL-1β levels, while increasing IFN-β, MX1, and OAS-1 mRNA expression. Conversely, overexpression of lncRNA-up4 led to increase IL-6, TNF-α, IL-1β, and decreased IFN-β, MX1, and OAS-1 levels. In conclusion, lncRNA-up4 modulates cytokines activity and inflammatory responses, providing insights into its regulatory role in innate immunity and interferon response against H9N2 IAV. This research enhances our understanding of the lncRNA-up4 regulatory network and its potential implication in inflammatory diseases.

ORGANISM(S): Gallus gallus

PROVIDER: GSE279270 | GEO | 2025/11/30

REPOSITORIES: GEO

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Project description:We aimed at systematically inferring the regulatory functions of host lncRNAs in response to influenza A virus (IAV) and severe acute respiratory syndrome coronavirus (SARS-CoV) in the mouse model, using a ‘guilt-by-association’ approach which relies on finding which lncRNAs have similar expression profiles to protein-coding genes of known function. To build a large panel of diverse host responses to viral infection, we took advantage of the genetic diversity present in the 8 founder strains of the Collaborative Cross (CC) mouse resource. Extensive pulmonary host-response profiling was performed on mock and viral-infected lungs at 2 and 4 days post-infection using total RNA-Seq. Overall lncRNAs accounted for about 40% of total genes differentially expressed upon infections (5,329 DE lncRNAs). To predict the functions of these lncRNAs, we constructed a co-expression network using the weighted correlation network analysis (WGCNA) and identified modules of co-expressed genes. Several lncRNAs were identified as belonging to gene modules associated with viral replication or weight loss, and enriched in various infection-related biological processes such as immune response. In addition, each lncRNA was individually annotated using ranked list of DE genes based on signed correlation with each LncRNA. We predicted that a few lncRNAs may be implicated in more than 50 biological processes or pathways. Finally, we identified the lncRNAs that were positively or negatively correlated with all their neighbors and may have cis enhancer or inhibitor effects. We validated our prediction by examining additional RNASeq dataset of mice treated with IFN-alpha. Altogether, these results provide a broad categorization of lncRNA functions and identify subsets of lncRNAs with potential key roles for respiratory virus pathogenesis. These data are fully accessible through The MOuse NOn-Code Lung database (MONOCLdb) http://monocldb.viromics.washington.edu/ At 2 or 4 days post infection, Collaborative Cross founders mice (n=2-3 for infected conditions, n=2 for mocks) were euthanized and lungs were used for total RNA-Seq.

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Identification of lncRNA-up4 as an Enhancer of Influenza A Virus Replication through Negatively Regulating the Innate Immune Response

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