Genome-wide maps of virus-induced transcription factors and transcription machinery at steady state and after virus infection

We report the application of high throughput sequencing technology for investigating the transcriptional regulatory network of the human innate immune response. With ChIP-seq, we generated genome-wide virus-activated transcription factor and transcription machinery maps of infected and uninfected human Namalwa B cells. Analysis of ChIP-seq data reveals extensive collaboration of IRF3 and NF-κB with Mediator throughout the human genome, and implicates additional transcription factor partners in antiviral responses. Moreover, analysis of Pol II occupancy and elongation status during virus infection indicates that IRF3 and NF-κB drive both de novo polymerase recruitment and mediate polymerase pause-release at their target sites, stimulating the expression of a variety of protein-coding, non-coding, and unannotated loci. Examination of 6 different proteins before and after virus infection in 1 cell type.