Jay’s interest in the way that bacterial pathogens cause disease in humans led him to begin working on Salmonella in 1990. He discovered that the H-NS protein is responsible for silencing gene expression in bacteria in 2006, and pioneered an approach that revealed a "snapshot" of bacterial gene expression during the process of infection of mammalian cells in 2003. Jay's team used RNA-seq-based approaches to understand the transcriptomic landscape of Salmonella Typhimurium, identifying 280 non-coding sRNAs and all active gene promoters. Jay’s research group is now using functional genomics to understand how new Salmonella pathovariants are causing endemic bloodstream infections across sub-Saharan Africa. This disease, iNTS, has killed around 500,000 people over the past decade. In 2018, they identified a specific genetic change, or single-nucleotide polymorphism (SNP), that helps one of the African Salmonella clades to survive in the human bloodstream. Jay's group recently discovered the evolutionary path taken by Salmonella over 50 years of human infections in Africa, and revealed the landmark genetic events responsible for shaping the phenotype of the pathogen. The Hinton lab is currently using a combination of RNA-seq-based transcriptomics, Tn-Seq/ TraDIS and experimental evolution to understand the infection biology of the dangerous African Salmonella pathovariants during infection of human macrophages. The underlying theme of current research is to understand the intricate interplay of gene function that leads to bacterial disease, to pave the way for new antibiotics and vaccines.