Welcome to the FluHit data exploration Shiny web interface

Influenza A viruses (IAV) use diverse mechanisms to interfere with cellular gene expression and thus limit the antiviral responses and/or promote viral replication. Although many RNAseq studies have documented IAV-induced changes in host mRNA abundance, few were designed to allow an accurate quantification of changes in host mRNA splicing. Here we show that IAV infection of human lung cells induces widespread alterations of cellular splicing, with an overall increase in exon inclusion and decrease in intron retention. Over half of the mRNAs that show differential splicing undergo no significant changes in abundance or in their 3’ end termination site, suggesting that IAV can directly manipulate cellular splicing independently of other transcriptional changes. Focusing on a subset of IAV-sensitive alternative splicing events, we found that most are conserved across distinct cell lines and viral subtypes, and are specific to IAV infection as they are not observed upon infection with VSV, induction of the interferon response or induction of an osmotic stress. Finally , cross-analysis of the alternative splicing profiles of IAV-infected and RED-depleted cells demonstrates a partial phenocopying of the RED-knock down phenotype in infected cells, suggesting that hijacking of the RED factor by IAVs to promote splicing of their own mRNAs could account for a minor subset of splicing changes in infected cells.

This Shiny Interface allow to explore the results presented in Ashraf et al (2020). Complete results of the different transcriptomic analysis are available: mutltivariate analysis (PCA), alternative splicing analysis with KisSplice, differential expression with DESeq2 and readthrough analysis.