As in all pathogenic bacteria, virulence of the facultative intracellular Listeria species is a multifactorial trait. The expression of the bacterial genes involved in the different steps of the infectious process--invasion, intracellular multiplication and spreading--is temporally and spatially controlled, thus ensuring the presence of the respective gene products at the right moment and place. So far, one network which is involved in the regulation of listerial virulence, the PrfA regulon, has been characterized rather well. The key element of this regulon, PrfA, belongs to the Crp/Fnr family of transcriptional regulators. Its synthesis and activity are influenced by a variety of physico-chemical signals outside and inside of eukaryotic host cells. The analysis of virulence gene expression in vivo, i.e. in infected host cells, indicates that yet uncharacterized bacterial factors other than PrfA, and possibly also host factors, modulate the expression of the PrfA regulon. Essentially nothing is known about the signal transduction pathways involved in the observed differential expression of virulence genes. Fermentable carbon sources seem to have a particular role in virulence gene regulation. In addition to the PrfA regulon, the Clp stress proteins have an impact on Listeria virulence. These two regulons interact with each other by an unknown mechanism.
- Bacterial Proteins/genetics
- Gene Expression Regulation, Bacterial
- Listeria monocytogenes/genetics
- Listeria monocytogenes/pathogenicity
- Molecular Chaperones
- Peptide Termination Factors