Research Brucella VirB And GntR In Intracellular Survival Of

Brucellosis is a worldwide zoonotic disease caused by Brucella pathogens, which lead to serious economic loss and public health risk. Brucella virulence factor VirB and regulator GntR have been proven to be the most important target genes and are playing important roles in regulated during the infectious process, both in promoting survival and thwarting host defenses, although the mechnisems are not very clear.The objective of this work was to understand the molecular mechanisms of VirB and GntR in brucella persist infection,which will advance our knowledge more deeply and promote our understanding of this pathogen infections. That will provide some potential candidates for new drug targets and potential protective antigens to develop new vaccines,and also give some new strategy in brucellosis provention.According to the many reports and results in brucella previous study, brucella16MAvirB and16MAgntR were reconstrcted using resistance replacement method. Brucella virulence phenotypes, the survival capabilities of the mutant under stress conditions simulating intracellular environments were tested.Some transcription of mutants genes involved in brucella regulater systems and metabolic pathways were verified by RT-PCRA deletion mutants of virB and GntR were successfully constructed. The deletion of genes of virB and gntR led the expression of the virB and gntR genes were inhibited in the mutants. Compared with the wild type strains, the mutants showed the speed of gowth and the survival capabilities under stress conditions were greatly decreased, implyed the genes virB and gntR are essential in intracellular survival and multiplication in under different stress conditions. The16M△virB transcription profiles of virulence genes, regulate genes(omp25, omp31, vjbR, gntR) under in vitro stress were analyzed by using quantitative RT-PCR and found that GntR as an inportant regulater was involved in biotin synthetic pasaway genes.In conclusion, virB and GntR are critical to their ability to produce chronic infections, bacterial virulence and metabolic pathway in brucella survival, which are plsy an inportant role in their mammalian hosts persistence infection and pathopoiesis.These findings of our work expand the VirB and GntR, which provide various important clues for the understanding of the molecular mechanism of intracellular survival of brucella. The paper serves deepen our understanding of those complex process and provide someclues in drug targets discover for brucella prevention and control.