Effect of Flavivirus infections (Kunjin, Zika, Yellow Fever) on gene expression and alternative splicing in U87 cells.
As obligate intracellular parasites, viruses rely heavily on their host cells for their replication, and therefore dysregulate several cellular processes for their benefit. In return, host cells activate multiple signaling pathways to limit viral replication and eradicate viruses. The present study explores the complex interplay between viruses and their host cells through next generation RNA sequencing. The coding transcriptome of human brain-derived U87 cells infected with Kunjin virus, Zika virus, or Yellow Fever virus were compared to the transcriptome of mock-infected cells. Changes in the abundance of several hundred mRNAs were found in each infection. Moreover, the alternative splicing of hundreds of mRNAs was found to be modulated upon viral infection. Overall design: U87 cells were either infected (MOI=5) or treated with cell-conditioned media for 24h (n=3 for each virus and control). PolyA-RNAs were extracted and sequenced. Differential gene expression analysis as well as differential alternative splicing analysis were performed using DESeq2 and rMATS, respectively.