An example is the hok/sok type I toxin-antitoxin system involved in the postsegregational killing mechanism employed by the R1 plasmid in E. coli. Conjugal transfer of pSLT is also controlled by a cisacting sRNA, namely FinP, which negatively regulates translation of the adjacent traJ gene. Most ABT-263 studies on sRNAs have been however conducted in the chromosome, overlooking the possible presence of these molecules in the virulence plasmid. A notable exception was a comprehensive RNAseq study focused in deciphering the transcriptional map of Salmonella plasmids during the early stationary phase of growth. The AZD6244 expression of these RNAs during infection conditions was, however, not examined. Manipulation of the relative levels of IesR-1 also led to alteration of virulence in the mouse typhoid model. Collectively, the data obtained in this work support a model involving a cis-acting mechanism of IesR-1 over PSLT047 with interaction at their respective 39 ends, a phenomenon that could modulate PSLT047 translation. This mechanism is consistent with the marked decrease of the PSLT047 protein observed in intracellular bacteria. Based on this observation, we next quantified the relative abundance of IesR-1 at different post-infection times upon bacterial entry into eukaryotic cells. NRK-49F rat fibroblasts, the host cells in which the Salgenomics microarray was used to obtain genome expression data of non-growing dormant intracellular bacteria, were infected to that purpose. Intracellular bacteria were collected at 1, 8 and 24 h post-infection and the transcript levels measured by RT-qPCR. IesR-1 levels increased notoriously upon infection of NRK-49F cells compared to the bacteria of the inoculum used to infect the fibroblasts. Computational, experimental and global RNAseq approaches have been used to search for non-coding regulatory sRNAs in S. Typhimurium. These studies have been mostly restricted to bacteria grown in vitro conditions, providing little insights into the transcription status during ex vivo or in vivo infections. A recent work in the mouse typhoid model in which S. Typhimurium mutants lacking defined sRNAs were used, uncovered the requirement of IstR, OxyS and SroA for virulence. Additional studies showed that the sRNAs IsrJ and IsrM contribute to invasion of epithelial cells and that S. Typhimurium also uses IsrM for proliferation in mouse organs. Apart from these studies, most sRNAs identified to date in S. Typhimurium remain to be shown whether they play a role in virulence. In this work, we focused on transcriptional changes in S. Typhimurium persisting within fibroblasts, a host cell type in which intracellular bacteria establish a non-proliferative, dormant state. Persistence is a strategy used by successful pathogens, including S. enterica, M. tuberculosis, or Helicobacter pylori among others. Our previous work demonstrated that certain S. Typhimurium sRNAs encoded in the chromosome exhibit unique expression pattern along the fibroblast infection. This observation is indicative of distinct time-dependent physiological roles for these molecules during progression of the persistence state. Here, we analyzed a novel S. Typhimurium sRNA encoded in the pSLT virulence plasmid that we named IesR-1. Besides FinP, IesR-1 would be the second example of a pSLT-encoded sRNA that, in this case, could have evolved to modulate the growth rate of the pathogen inside the eukaryotic cell. Interestingly, other functions encoded in the pSLT plasmid, such as the transcriptional regulator SpvR, are induced in a Caenorhabditis elegans persistent infection model. Although pSLT is known to be required for Salmonella virulence, little is known about additional regulatory molecules encoded by this plasmid playing a role in pathogen persistence.