A ROD9 island encoded gene in Salmonella Enteritidis plays an important role in acid tolerance response and helps in systemic infection in mice.

, like other pathogenic bacteria has undergone multiple genomic alterations to adapt itself into specific host environments executing varied degrees of virulence through evolution. Such variations in genome content have been assumed to lead the closely related non-typhoidal serovars, . Enteritidis, and . Typhimurium to exhibit Type Three Secretion System -2 (T3SS-2) based diverse colonization and inflammation kinetics. Mutually exclusive genes present in either of the serovars are recently being studied and in our currentwork, we focused on a particular island ROD9, present in . Enteritidis but not in . Typhimurium. Earlier reports have identified a few genes from this island to be responsible for virulence as well as . In this study, we have identified another gene, from the same island encoding a hypothetical protein to be a potential virulence determinant showing systemic attenuation upon mutation in C57BL/6 mice infection model. The isogenic mutant strain displayed reduced adhesion to epithelial cells as well as was highly immotile. It was also deficient in intracellular replication , with a highly suppressed SPI-2and failed to cause acute colitis at 72-h p.i.. Moreover, on acid exposure, showed 17 folds and 2 fold up-regulations during adaptation and challenge phases,respectively and Δ failed to survive during ATR assay, indicating its role under acid stress. Together, our findings suggested Δ to be significantly attenuated and we propose this gene to be a potent factor responsible for . Enteritidis pathogenesis.