Member of the two-component regulatory system SsrA/SsrB (SpiR/SsrB) that is required for intracellular proliferation and systemic dissemination within the host. When inside acidic Salmonella-containing vesicles (SCV) within host cells the SsrA sensor kinase autophosphorylates and the phosphoryl group is transferred to the response regulator SsrB; phosphorylated SsrB activates the expression of genes encoding virulence proteins, including pathogenicity island 2 (SPI2) and other horizontally acquired genes, but also ancestral genes; it can stimulate gene expression both by recruiting RNA polymerase and by antagonizing the action of the transcriptional repressor hns (H-NS). Can also act independently of sensor kinase ssrA to support the dormant carrier state by directing the transcription of factors required for biofilm formation. DNA-binding is stimulated by acidic pH conditions, and binding promotes bending of DNA both upstream and downstream of binding sites. Binds a degenerate 18-basepair palindromic sequence with a 7-4-7 internal organization, and regulates gene expression from 86 operons. When phosphorylated, activates the transcription of the ABC transporter complex dalSTUV, which helps protect the organism from oxidative killing by host neutrophils. Binds the phoP promoter to stimulate expression in acidic pH conditions. Antagonizes hns to activate the transcription of ugtL. Following invasion of host cells, binds the hilD and hilA regulatory regions to repress their transcription and consequently to repress transcription of pathogenicity island 1 (SPI1) encoding genes involved in host cell invasion. Binds the promoters of the flagellar master regulators flhD and flhC to repress their expression and consequently to suppress flagellar motility and promote evasion of the host inflammasome during infection of host cells. Activates expression of sseI/srfH, sifA, sifB, sseJ and regulates its own expression. When unphosphorylated, relieves the hns-mediated repression of master biofilm regulator csgD by binding and bending the csgD regulatory region. May act as early as in the lumen of the host small intestine, to activate the expression of virulence proteins prior to invasion of host cells