Signal transduction and virulence regulation in human and animal pathogens

Abstract

Pathogens have developed many strategies for survival in animals and humans which possess very effective defense mechanisms. Although there are many different ways, in which pathogenic bacteria solved the problem to overcome the host defense, some common features of virulence mechanisms can be detected even in phylogenetically very distant bacteria (Finlay and Falkow (1989) Microb. Rev. 6 1375–1383). One important feature is that the regulation of expression of virulence factors and the exact timing of their expression is very important for many of the pathogenic bacteria, as most of them have to encounter different growth situations during an infection cycle, which require a fast adaptation to the new situation by the expression of different factors. This review gives an overview about the mechanisms used by pathogenic bacteria to accomplish the difficult task of regulation of their virulence potential in response to environmental changes. In addition, the relationship of these virulence regulatory systems with other signal transduction mechanisms not involved in pathogenicity is discussed.

Unraveling the Microbial Interactions and Metabolic Potentials in Pre- and Post-treated Sludge from a Wastewater Treatment Plant Using Metagenomic Studies

“…The number of reads belonging to flagellar movement and chemotaxis were relatively abundant in RS which illustrate the need to cut down the pathogenicity levels. Signal transduction networks are one of the essential factors that regulate the virulence factors in pathogenic bacteria and make them competent to survive in the adverse conditions (Gross, 1993). Reads mapped to signal transduction genes were also found to be relatively abundant in RS which once again gives us insights into the virulence of RS.…”

Dual input control: activation of the Bartonella henselae VirB/D4 type IV secretion system by the stringent sigma factor RpoH1 and the BatR/BatS two‐component system

“…The co-ordinated expression of virulence factors during the progression of the infection cycle is an essential aspect of bacterial pathogenicity and a prerequisite for successful host-adaptation (Gross, 1993;Cotter and DiRita, 2000;Beier and Gross, 2006;Boutte and Crosson, 2013). The stringent response (SR) represents a prominent adaptive response mechanism that has been recruited by bacterial pathogens to respond to the microenvironments encountered in the host and to control expression of their virulence factors (Dalebroux et al, 2010).…”

Specificity of the BvgAS and EvgAS phosphorelay is mediated by the C‐terminal HPt domains of the sensor proteins

“…Both systems show very significant sequence similarities even outside of the conserved signalling modules and, accordingly, seem to respond to similar external stimuli Utsumi et al, 1994;. Whereas the function of the Evg system is not known, the Bvg system is the master regulator of virulence in B. pertussis, the aetiological agent of whooping cough (Bordet and Gengou, 1909;Weiss and Hewlett, 1986;Scarlato et al, 1991;Gross, 1993;Uhl and Miller, 1994). Recently, it has been shown that, similar to the Bacillus and Saccharomyces systems, a complex phosphorelay occurs that involves the autophosphorylation of the BvgS transmitter (His-729) and subsequent phosphorylation of Asp-1023 in its receiver and of His-1172 in its HPt domain before the phosphorylation of BvgA (Uhl and Miller, 1994;1996a).…”