As in all pathogenic bacteria, virulence of the facultative intracellular L
isteria 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 c
ontrolled, thus ensuring the presence of the respective gene products at th
e right moment and place. So far, one network which is involved in the regu
lation of listerial virulence, the PrfA regulon, has been characterized rat
her well. The key element of this regulon, PrfA, belongs to the Crp/Fnr fam
ily of transcriptional regulators. Its synthesis and activity are influence
d 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 inf
ected host cells, indicates that yet uncharacterized bacterial factors othe
r than PrfA, and possibly also host factors, modulate the expression of the
PrfA regulon. Essentially nothing is known about the signal transduction p
athways involved in the observed differential expression of virulence genes
. Fermentable carbon sources seem to have a particular role in virulence ge
ne regulation. In addition to the PrfA regulon, the Clp stress proteins hav
e an impact on Listeria virulence. These two regulons interact with each ot
her by an unknown mechanism.