Disease relevance of vrg-6

• The Bordetella virulence control locus, bvgAS, activates and represses gene expression in response to environmental signals [1].
• Virulence factors of Bordetella bronchiseptica associated with the production of infectious atrophic rhinitis and pneumonia in experimentally infected neonatal swine [2].
• Virulence of Streptococcus suis type 2 strains in newborn germfree pigs depends on phenotype [3].
• Pertussis toxin (PT), a virulence factor secreted by Bordetella pertussis, contributes to respiratory tract infection and disease caused by this pathogen [4].
• Comparative analysis of Bvg regulation in B. pertussis and B. bronchiseptica revealed a relatively conserved Bvg(+) phase transcriptional program and identified previously uncharacterized candidate virulence factors [5].

High impact information on vrg-6

• While infection requires virulence gene activation, the role of gene repression during infection is not understood [1].
• Type III secretion mutants also showed increased lethal virulence in immunodeficient SCID-beige mice [6].
• Functional BvgAS virulence control system in Bordetella bronchiseptica is necessary for induction of Ca2+ transients in ciliated tracheal epithelial cells [7].
• It produces several purported virulence factors, including the dermonecrotic toxin (DNT), which has been implicated in the turbinate atrophy seen in cases of atrophic rhinitis [8].
• The virulence of the alcA mutant in colostrum-deprived, caesarean-delivered piglets was compared with that of the parent strain in two experiments [9].

Chemical compound and disease context of vrg-6

• Virulence of Bordetella bronchiseptica: role of adenylate cyclase-hemolysin [10].
• Moreover, a negative effect of slight overexpression of CspB, but not of the other CSPs, on the transcription of the adenylate cyclase toxin CyaA of Bordetella pertussis was observed, suggesting cross-talk between the CSP-mediated stress response stimulon and the Bordetella virulence regulon [11].
• Bordetella Bronchiseptica Dermonecrotoxin (BBD) as a major virulence factor of a causative agent of atrophic rhinitis (AR) was loaded to the chitosan microspheres for vaccination [12].

Biological context of vrg-6

• A majority of the virulence factors expressed by these bacteria are regulated by a master control locus, BvgAS, a member of the two-component family of signal transduction systems [13].
• Plasmids were detected in only five of the strains which induced ciliostasis, transfer of plasmids from four of these strains to one which did not induce ciliostasis did not alter its virulence or colony morphology [14].
• Pathogenic virulence factors can inhibit defensin gene expression, as can environmental factors such as air pollution [15].
• The virulence of Bordetella bronchiseptica in gnotobiotic piglets was studied by intranasal infection with 11 cultures derived from eight strains isolated from pigs (4), dogs (2), a human subject and a monkey [16].
• Flagellin is encoded by a vrg gene, which is expressed when the principal virulence factors are eliminated during antigenic modulation or in phase variants (Akerley et al., 1992) [17].

Anatomical context of vrg-6

• Virulence was studied by transmission of vaccinal strain through 3 serial growing passages on the nasal mucosa of a litter of hysterectomy-produced colostrum-deprived pigs [18].

Associations of vrg-6 with chemical compounds

• Western blot analysis demonstrated that virulence factors, filamentous hemagglutinin, pertactin, and adenylate cyclase toxin are produced by the sea otter B. bronchiseptica isolate [19].
• In addition to the effects of these drugs on some putative virulence factors, we suggest that the strong PAEs caused by tilmicosin, tylosin, and apramycin may also contribute to the in vivo efficacy of these drugs [20].
• The in vitro effect of tilmicosin, tylosin, and apramycin (even when used at sub-MIC levels) on growth, production of capsular material, and haemolytic activity might impair the virulence of some of the microorganisms studied [20].
• Production of this cytotoxic activity appeared to be regulated by the BvgAS sensory transduction system, which coordinately regulates many B. bronchiseptica virulence factors, since bacteria cultured in the presence of sulfate anions, inhibitors of the BvgAS response, did not exhibit this effect [21].
• METHODS AND RESULTS: Congo red binding and urease activity of Bvg+ B. bronchiseptica cultures in different liquid media were compared with the expression of virulence markers such as filamentous haemagglutinin and some outer membrane proteins (OMP) [22].

Other interactions of vrg-6

• Bordetella bronchiseptica infection requires the activation of virulence genes by the two-component BvgAS regulatory system, which also activates bvgR, a repressor of another set of genes called avirulence genes [23].
• The fact that the most virulent isolate did not express dermonecrotic toxin suggests that this toxin does not play an important role in the virulence of the bacteria in the murine model [10].

Analytical, diagnostic and therapeutic context of vrg-6

• Bordetella Bronchiseptica Dermonecrotoxin (BBD), a major virulence factor of a causative agent of atrophic rhinitis (AR), was loaded on to the CMs for nasal vaccination [24].
• The virulence of 11 strains of P multocida was investigated by intraperitoneal injection of culture filtrates in BALB/C mice, or by infection of gnotobiotic piglets given B bronchiseptica five days previously [25].

References