Journal articles on the topic 'Virulent factors'
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1
Tan, Y. P., Q. Lin, X. H. Wang, S. Joshi, C. L. Hew, and K. Y. Leung. "Comparative Proteomic Analysis of Extracellular Proteins of Edwardsiella tarda." Infection and Immunity 70, no. 11 (November 2002): 6475–80. http://dx.doi.org/10.1128/iai.70.11.6475-6480.2002.
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ABSTRACT A comparison of extracellular proteins of virulent and avirulent Edwardsiella tarda strains revealed several major, virulent-strain-specific proteins. Proteomic analysis identified two of the proteins in the virulent strain PPD130/91 as flagellin and SseB, which are virulence factors in bacterial pathogens. PCR amplification and DNA sequencing confirmed the presence of the genes that encode these proteins. Our results clearly demonstrated the potency of the proteomic approach in identifying virulence factors.
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ERDENLIG, SEVIL, A. JERALD AINSWORTH, and FRANK W. AUSTIN. "Pathogenicity and Production of Virulence Factors by Listeria monocytogenes Isolates from Channel Catfish." Journal of Food Protection 63, no. 5 (May 1, 2000): 613–19. http://dx.doi.org/10.4315/0362-028x-63.5.613.
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Pathogenicity of four channel catfish Listeria monocytogenes isolates (CCF1, CCF4, HCC7, and HCC23) was examined in a comparative manner with virulent type strains L. monocytogenes ATCC 19115 and EGD and avirulent type strain ATCC 15313 in BDF and A/J mice. Isolates HCC7 and CCF1 (both serovar 1) caused similar percent mortalities and 50% lethal concentration values when compared with virulent type strains and were therefore considered pathogenic. The presence of the virulence factors listeriolysin (LLO), phosphotidylcholine-phospholipase (PC-PLC), and phosphotidylinositol-phospholipase (PI-PLC) was determined using specific activity tests. The virulent catfish isolates were positive for production of LLO, PCPLC, and PI-PLC. However, catfish isolate HCC23 was not virulent in mice despite being hemolytic, suggesting that not every hemolytic L. monocytogenes strain is virulent. With the exception of HCC7, all virulent strains displayed enhanced LLO production in a special stress medium, whereas almost undetectable LLO activity was present when catfish isolates and virulent type strain L. monocytogenes were grown in a rich medium such as brain heart infusion. Avirulent strains were found to lack or have decreased expression of LLO, PC-PLC, or PI-PLC.
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Grim, Christopher J., Elena V. Kozlova, Duraisamy Ponnusamy, Eric C. Fitts, Jian Sha, Michelle L. Kirtley, Christina J. van Lier, et al. "Functional Genomic Characterization of Virulence Factors from Necrotizing Fasciitis-Causing Strains of Aeromonas hydrophila." Applied and Environmental Microbiology 80, no. 14 (May 2, 2014): 4162–83. http://dx.doi.org/10.1128/aem.00486-14.
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ABSTRACTThe genomes of 10Aeromonasisolates identified and designatedAeromonas hydrophilaWI, Riv3, and NF1 to NF4;A. dhakensisSSU;A. jandaeiRiv2; andA. caviaeNM22 and NM33 were sequenced and annotated. Isolates NF1 to NF4 were from a patient with necrotizing fasciitis (NF). Two environmental isolates (Riv2 and -3) were from the river water from which the NF patient acquired the infection. While isolates NF2 to NF4 were clonal, NF1 was genetically distinct. Outside the conserved core genomes of these 10 isolates, several unique genomic features were identified. The most virulent strains possessed one of the following four virulence factors or a combination of them: cytotoxic enterotoxin, exotoxin A, and type 3 and 6 secretion system effectors AexU and Hcp. In a septicemic-mouse model, SSU, NF1, and Riv2 were the most virulent, while NF2 was moderately virulent. These data correlated with high motility and biofilm formation by the former three isolates. Conversely, in a mouse model of intramuscular infection, NF2 was much more virulent than NF1. Isolates NF2, SSU, and Riv2 disseminated in high numbers from the muscular tissue to the visceral organs of mice, while NF1 reached the liver and spleen in relatively lower numbers on the basis of colony counting and tracking of bioluminescent strains in real time byin vivoimaging. Histopathologically, degeneration of myofibers with significant infiltration of polymorphonuclear cells due to the highly virulent strains was noted. Functional genomic analysis provided data that allowed us to correlate the highly infectious nature ofAeromonaspathotypes belonging to several different species with virulence signatures and their potential ability to cause NF.
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França, Angela, Vânia Gaio, Nathalie Lopes, and Luís D. R. Melo. "Virulence Factors in Coagulase-Negative Staphylococci." Pathogens 10, no. 2 (February 4, 2021): 170. http://dx.doi.org/10.3390/pathogens10020170.
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Coagulase-negative staphylococci (CoNS) have emerged as major pathogens in healthcare-associated facilities, being S. epidermidis, S. haemolyticus and, more recently, S. lugdunensis, the most clinically relevant species. Despite being less virulent than the well-studied pathogen S. aureus, the number of CoNS strains sequenced is constantly increasing and, with that, the number of virulence factors identified in those strains. In this regard, biofilm formation is considered the most important. Besides virulence factors, the presence of several antibiotic-resistance genes identified in CoNS is worrisome and makes treatment very challenging. In this review, we analyzed the different aspects involved in CoNS virulence and their impact on health and food.
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Mroczyńska, Martyna, and Anna Brillowska-Dąbrowska. "Virulence of Clinical Candida Isolates." Pathogens 10, no. 4 (April 12, 2021): 466. http://dx.doi.org/10.3390/pathogens10040466.
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The factors enabling Candida spp. infections are secretion of hydrolytic enzymes, adherence to surfaces, biofilm formation or morphological transition, and fitness attributes. The aim of this study was to investigate the correlation between known extracellular virulence factors and survival of Galleria mellonella larvae infected with clinical Candida. The 25 isolates were tested and the activity of proteinases among 24/24, phospholipases among 7/22, esterases among 14/23, hemolysins among 18/24, and biofilm formation ability among 18/25 isolates was confirmed. Pathogenicity investigation using G. mellonella larvae as host model demonstrated that C. albicans isolates and C. glabrata isolate were the most virulent and C. krusei isolates were avirulent. C. parapsilosis virulence was identified as varied, C. inconspicua were moderately virulent, and one C. palmioleophila isolate was of low virulence and the remaining isolates of this species were moderately virulent. According to our study, virulence of Candida isolates is related to the expression of proteases, hemolysins, and esterases.
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de Leeuw, Olav S., Guus Koch, Leo Hartog, Niek Ravenshorst, and Ben P. H. Peeters. "Virulence of Newcastle disease virus is determined by the cleavage site of the fusion protein and by both the stem region and globular head of the haemagglutinin–neuraminidase protein." Journal of General Virology 86, no. 6 (June 1, 2005): 1759–69. http://dx.doi.org/10.1099/vir.0.80822-0.
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Virulence of Newcastle disease virus (NDV) is mainly determined by the amino acid sequence surrounding the fusion (F) protein cleavage site, since host proteases that cleave the F protein of virulent strains are present in more tissues than those that cleave the F protein of non-virulent strains. Nevertheless, comparison of NDV strains that carry exactly the same F protein cleavage site shows that significant differences in virulence still exist. For instance, virulent field strain Herts/33 with the F cleavage site 112RRQRRF117 had an intracerebral pathogenicity index of 1·88 compared with 1·28 for strain NDFLtag, which has the same cleavage site. This implies that additional factors contribute to virulence. After generating an infectious clone of Herts/33 (FL-Herts), we were able to map the location of additional virulence factors by exchanging sequences between FL-Herts and NDFLtag. The results showed that, in addition to the F protein cleavage site, the haemagglutinin–neuraminidase (HN) protein also contributed to virulence. The effect of the HN protein on virulence was most prominent after intravenous inoculation. Interestingly, both the stem region and the globular head of the HN protein seem to be involved in determining virulence.
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Uzelac, Aleksandra, Ivana Klun, Vladimir Ćirković, and Olgica Djurković-Djaković. "In Vivo and In Vitro Virulence Analysis of Four Genetically Distinct Toxoplasma gondii Lineage III Isolates." Microorganisms 8, no. 11 (October 31, 2020): 1702. http://dx.doi.org/10.3390/microorganisms8111702.
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Toxoplasma gondii archetypes II and III are mildly virulent, yet virulence of variant strains is largely unknown. While lineage II dominates in humans in Europe, lineage III strains are present in various intermediate hosts. In Serbia, lineage III represents 24% of the population structure and occurs most frequently in domestic animals, implying a significant presence in the human food web. In this study, the virulence of four genetically distinct lineage III variants was assessed in vivo and in vitro. In vivo, two strains were shown to be intermediately virulent and two mildly virulent, with cumulative mortalities of 69.4%, 38.8%, 10.7%, and 6.8%, respectively. The strain with the highest mortality has previously been isolated in Europe and may be endemic; the strain with the lowest mortality matches ToxoDB#54, while the remaining two represent novel genotypes. Identical alleles were detected at ROP5, ROP16, ROP18, and GRA15. A set of in vitro analyses revealed proliferation and plaque formation as virulence factors. Higher levels of expression of ENO2 in intermediately virulent strains point to enhanced metabolism as the underlying mechanism. The results suggest that metabolic attenuation, and possibly stage conversion, may be delayed in virulent strains.
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Chiu, Yi-Chun, Wei-Chen Tai, Seng-Kee Chuah, Ping-I. Hsu, Deng-Chyang Wu, Keng-Liang Wu, Chao-Cheng Huang, Ji-Chen Ho, Johannes Ring, and Wen-Chieh Chen. "The Clinical Correlations ofHelicobacter pyloriVirulence Factors and Chronic Spontaneous Urticaria." Gastroenterology Research and Practice 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/436727.
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Background and Study Aims. The association betweenHelicobacter pylori(H. pylori) and chronic spontaneous urticaria (CSU) remains controversial. This study explored the role ofH. pyloriin CSU among different virulent genotypes patients.Patients and Methods. Patients infected byH. pyloriwere sorted into two groups as group A (with CSU) and group B (without CSU). The tissue materials were taken via endoscopy for polymerase chain reaction study to determine virulence factors.AfterH. pylorieradication therapy, the eradication rate and response of urticaria were evaluated by using C13-UBT and a three-point scale (complete remission, partial remission, or no improvement).Results. The results were comparable between patients of groups A and B in terms ofH. pyloriinfection rates and eradication rate. Longitudinal follow-up of 23.5 months showed complete remission of urticaria in 63.6% but no improvement in 36.4% of the patients afterH. pylorieradication.H. pyloriinfected patients with different virulence factors such as cytotoxin-associated gene A, vacuolating cytotoxin gene A signal region and middle region have similar remission rates for CSU.Conclusions. Current study suggests thatH. pylorimay play a role in the development and disease course of CSU but may be irrelevant to different virulent genotypes.
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Beach, Nathan M., Robert B. Duncan, Calvert T. Larsen, Xiang-Jin Meng, Nammalwar Sriranganathan, and F. William Pierson. "Comparison of 12 turkey hemorrhagic enteritis virus isolates allows prediction of genetic factors affecting virulence." Journal of General Virology 90, no. 8 (August 1, 2009): 1978–85. http://dx.doi.org/10.1099/vir.0.010090-0.
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Turkey hemorrhagic enteritis virus (THEV) is a member of the genus Siadenovirus and causes disease in turkey poults characterized by splenomegaly, bloody diarrhoea and death. The mechanism responsible for intestinal lesion formation and mortality is not known, although there is strong evidence that it is immune-mediated. All strains of THEV are serologically indistinguishable, although there are naturally occurring avirulent strains of THEV that replicate efficiently in turkeys without the intestinal haemorrhage or mortality associated with more virulent strains. The purpose of this study was to determine which viral genes are involved in virulence. The full-length genome of an avirulent vaccine strain was sequenced and compared with the genome of a virulent field isolate from Israel that was sequenced in 1998. Comparison of the two 26.3 kb genomes revealed 49 nucleotide differences resulting in 14 putative amino acid changes within viral proteins. Sequencing of the regions surrounding the 14 missense mutations revealed variations in ORF1, E3 and the fiber (fib) knob domain in five additional strains with varying degrees of virulence. Complete sequences of these genes were determined in a total of 11 different strains of THEV. All strains had at least one missense mutation in ORF1, and all but two of the strains had one missense mutation in E3. At least one missense mutation was found in the fiber knob domain in six out of seven virulent strains. Sequence variation of ORF1, E3 and fib in strains of THEV with different phenotypes strongly indicates that these genes are the key factors affecting virulence.
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Susič, Nik, Sandra Janežič, Maja Rupnik, and Barbara Gerič Stare. "Whole Genome Sequencing and Comparative Genomics of Two Nematicidal Bacillus Strains Reveals a Wide Range of Possible Virulence Factors." G3: Genes|Genomes|Genetics 10, no. 3 (January 9, 2020): 881–90. http://dx.doi.org/10.1534/g3.119.400716.
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Bacillus firmus nematicidal bacterial strains are used to control plant parasitic nematode infestation of crops in agricultural production. Proteases are presumed to be the primary nematode virulence factors in nematicidal B. firmus degrading the nematode cuticle and other organs. We determined and compared the whole genome sequences of two nematicidal strains. Comparative genomics with a particular focus on possible virulence determinants revealed a wider range of possible virulence factors in a B. firmus isolate from a commercial bionematicide and a wild type Bacillus sp. isolate with nematicidal activity. The resulting 4.6 Mb B. firmus I-1582 and 5.3 Mb Bacillus sp. ZZV12-4809 genome assemblies contain respectively 18 and 19 homologs to nematode-virulent proteases, two nematode-virulent chitinase homologs in ZZV12-4809 and 28 and 36 secondary metabolite biosynthetic clusters, projected to encode antibiotics, small peptides, toxins and siderophores. The results of this study point to the genetic capability of B. firmus and related species for nematode virulence through a range of direct and indirect mechanisms.
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Wang, Yu, Kazuo Suzuki, Daisuke Sakaue, and Toshihiro Yamada. "Variations in life history parameters and their influence on rate of population increase of different pathogenic isolates of the pine wood nematode, Bursaphelenchus xylophilus." Nematology 7, no. 3 (2005): 459–67. http://dx.doi.org/10.1163/156854105774355545.
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AbstractTwo virulent isolates and two avirulent isolates of Bursaphelenchus xylophilus and one isolate of B. mucronatus were used to investigate the relationships between life history parameters, rate of population increase and virulence. The results showed that on fungal cultures of Botrytis cinerea, virulent B. xylophilus completed one generation much faster than did avirulent B. xylophilus and B. mucronatus. There was a tendency that virulent B. xylophilus isolates laid more eggs during the egg laying period than did avirulent populations. Shorter generation time and higher fecundity resulted in a higher rate of population increase. Generation time and fecundity were primary factors determining rate of population increase. Difference in rate of population increase is closely related to variation of virulence: virulent B. xylophilus increased population size at the fastest rate, avirulent B. xylophilus was slower, and B. mucronatus was slowest. It is assumed that similar variations in life history parameters and rate of population increase are also expressed in pine trees and help to explain variation of virulence in the field.
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El-Helw, H. A., M. M. Taha, Elham F. El-Sergany, Ebtesam, E. Z. Kotb, A. S. Hussein, and Y. A. Abdalla. "Identifying the Virulent Factors of Clostridium perfringens Locally Isolated from Different Species." World's Veterinary Journal 10, no. 4 (December 25, 2020): 617–24. http://dx.doi.org/10.54203/scil.2020.wvj74.
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Clostridium perfringens incriminated in many diseases among different species of animals due to its ability to produce many virulence factors. In the current study, 135 intestinal samples were collected from different animal species of different localities in Egypt. Samples were subjected to isolation and identification (morphologically and biochemically) for obtaining Clostridium perfringens isolates (n=26, 19.25%). The PCR was carried out to elucidate the virulence factors. It was indicated that all the 26 Clostridium perfringens isolates had CPA gene and Clostridium perfringens enterotoxin (CPE gene), whereas 23% of isolates of chicken and cattle intestinal samples contained CPA, Net B, and CPE genes as virulence factors. Consequently, those isolates are highly recommended to be used in the preparation of enterotoxemia and necrotic enteritis vaccines as they are more virulent strains.
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Li, Sha, Liurong Fang, Wei Liu, Tao Song, Fuwei Zhao, Ruoxi Zhang, Dang Wang, and Shaobo Xiao. "Quantitative Proteomic Analyses of a Pathogenic Strain and Its Highly Passaged Attenuated Strain ofMycoplasma hyopneumoniae." BioMed Research International 2019 (July 1, 2019): 1–18. http://dx.doi.org/10.1155/2019/4165735.
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Mycoplasma hyopneumoniaeis the causative agent of porcine enzootic pneumonia, a chronic respiratory disease in swine resulting in enormous economic losses. To identify the components that contribute to virulence and unveil those biological processes potentially related to attenuation, we used isobaric tags for relative and absolute quantification technology (iTRAQ) to compare the protein profiles of the virulentM. hyopneumoniaestrain 168 and its attenuated highly passaged strain 168L. We identified 489 proteins in total, 70 of which showing significant differences in level of expression between the two strains. Remarkably, proteins participating in inositol phosphate metabolism were significantly downregulated in the virulent strain, while some proteins involved in nucleoside metabolism were upregulated. We also mined a series of novel promising virulence-associated factors in our study compared with those in previous reports, such as some moonlighting adhesins, transporters, lipoate-protein ligase, and ribonuclease and several hypothetical proteins with conserved functional domains, deserving further research. Our survey constitutes an iTRAQ-based comparative proteomic analysis of a virulentM. hyopneumoniaestrain and its attenuated strain originating from a single parent with a well-characterized genetic background and lays the groundwork for future work to mine for potential virulence factors and identify candidate vaccine proteins.
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Djukic, Marvin, Silvio Erler, Andreas Leimbach, Daniela Grossar, Jean-Daniel Charrière, Laurent Gauthier, Denise Hartken, et al. "Comparative Genomics and Description of Putative Virulence Factors of Melissococcus plutonius, the Causative Agent of European Foulbrood Disease in Honey Bees." Genes 9, no. 8 (August 20, 2018): 419. http://dx.doi.org/10.3390/genes9080419.
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In Europe, approximately 84% of cultivated crop species depend on insect pollinators, mainly bees. Apis mellifera (the Western honey bee) is the most important commercial pollinator worldwide. The Gram-positive bacterium Melissococcus plutonius is the causative agent of European foulbrood (EFB), a global honey bee brood disease. In order to detect putative virulence factors, we sequenced and analyzed the genomes of 14 M. plutonius strains, including two reference isolates. The isolates do not show a high diversity in genome size or number of predicted protein-encoding genes, ranging from 2.021 to 2.101 Mbp and 1589 to 1686, respectively. Comparative genomics detected genes that might play a role in EFB pathogenesis and ultimately in the death of the honey bee larvae. These include bacteriocins, bacteria cell surface- and host cell adhesion-associated proteins, an enterococcal polysaccharide antigen, an epsilon toxin, proteolytic enzymes, and capsule-associated proteins. In vivo expression of three putative virulence factors (endo-alpha-N-acetylgalactosaminidase, enhancin and epsilon toxin) was verified using naturally infected larvae. With our strain collection, we show for the first time that genomic differences exist between non-virulent and virulent typical strains, as well as a highly virulent atypical strain, that may contribute to the virulence of M. plutonius. Finally, we also detected a high number of conserved pseudogenes (75 to 156) per genome, which indicates genomic reduction during evolutionary host adaptation.
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Belibasakis, Maula, Bao, Lindholm, Bostanci, Oscarsson, Ihalin, and Johansson. "Virulence and Pathogenicity Properties of Aggregatibacter actinomycetemcomitans." Pathogens 8, no. 4 (November 6, 2019): 222. http://dx.doi.org/10.3390/pathogens8040222.
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Aggregatibacter actinomycetemcomitans is a periodontal pathogen colonizing the oral cavity of a large proportion of the human population. It is equipped with several potent virulence factors that can cause cell death and induce or evade inflammation. Because of the large genetic diversity within the species, both harmless and highly virulent genotypes of the bacterium have emerged. The oral condition and age, as well as the geographic origin of the individual, influence the risk to be colonized by a virulent genotype of the bacterium. In the present review, the virulence and pathogenicity properties of A. actinomycetemcomitans will be addressed.
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Sharma-Poudyal, D., X. M. Chen, A. M. Wan, G. M. Zhan, Z. S. Kang, S. Q. Cao, S. L. Jin, et al. "Virulence Characterization of International Collections of the Wheat Stripe Rust Pathogen, Puccinia striiformis f. sp. tritici." Plant Disease 97, no. 3 (March 2013): 379–86. http://dx.doi.org/10.1094/pdis-01-12-0078-re.
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Wheat stripe rust (yellow rust [Yr]), caused by Puccinia striiformis f. sp. tritici, is an economically important disease of wheat worldwide. Virulence information on P. striiformis f. sp. tritici populations is important to implement effective disease control with resistant cultivars. In total, 235 P. striiformis f. sp. tritici isolates from Algeria, Australia, Canada, Chile, China, Hungary, Kenya, Nepal, Pakistan, Russia, Spain, Turkey, and Uzbekistan were tested on 20 single Yr-gene lines and the 20 wheat genotypes that are used to differentiate P. striiformis f. sp. tritici races in the United States. The 235 isolates were identified as 129 virulence patterns on the single-gene lines and 169 virulence patterns on the U.S. differentials. Virulences to YrA, Yr2, Yr6, Yr7, Yr8, Yr9, Yr17, Yr25, YrUkn, Yr28, Yr31, YrExp2, Lemhi (Yr21), Paha (YrPa1, YrPa2, YrPa3), Druchamp (Yr3a, YrD, YrDru), Produra (YrPr1, YrPr2), Stephens (Yr3a, YrS, YrSte), Lee (Yr7, Yr22, Yr23), Fielder (Yr6, Yr20), Tyee (YrTye), Tres (YrTr1, YrTr2), Express (YrExp1, YrExp2), Clement (Yr9, YrCle), and Compair (Yr8, Yr19) were detected in all countries. At least 80% of the isolates were virulent on YrA, Yr2, Yr6, Yr7, Yr8, Yr17, YrUkn, Yr31, YrExp2, Yr21, Stephens (Yr3a, YrS, YrSte), Lee (Yr7, Yr22, Yr23), and Fielder (Yr6, Yr20). Virulences to Yr1, Yr9, Yr25, Yr27, Yr28, Heines VII (Yr2, YrHVII), Paha (YrPa1, YrPa2, YrPa3), Druchamp (Yr3a, YrD, YrDru), Produra (YrPr1, YrPr2), Yamhill (Yr2, Yr4a, YrYam), Tyee (YrTye), Tres (YrTr1, YrTr2), Hyak (Yr17, YrTye), Express (YrExp1, YrExp2), Clement (Yr9, YrCle), and Compair (Yr8, Yr19) were moderately frequent (>20 to <80%). Virulence to Yr10, Yr24, Yr32, YrSP, and Moro (Yr10, YrMor) was low (≤20%). Virulence to Moro was absent in Algeria, Australia, Canada, Kenya, Russia, Spain, Turkey, and China, but 5% of the Chinese isolates were virulent to Yr10. None of the isolates from Algeria, Canada, China, Kenya, Russia, and Spain was virulent to Yr24; none of the isolates from Algeria, Australia, Canada, Nepal, Russia, and Spain was virulent to Yr32; none of the isolates from Australia, Canada, Chile, Hungary, Kenya, Kenya, Nepal, Pakistan, Russia, and Spain was virulent to YrSP; and none of the isolates from any country was virulent to Yr5 and Yr15. Although the frequencies of virulence factors were different, most of the P. striiformis f. sp. tritici isolates from these countries shared common virulence factors. The virulences and their frequencies and distributions should be useful in breeding stripe-rust-resistant wheat cultivars and understanding the pathogen migration and evolution.
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Dortmans, J. C. F. M., G. Koch, P. J. M. Rottier, and B. P. H. Peeters. "Virulence of pigeon paramyxovirus type 1 does not always correlate with the cleavability of its fusion protein." Journal of General Virology 90, no. 11 (November 1, 2009): 2746–50. http://dx.doi.org/10.1099/vir.0.014118-0.
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Some pigeon paramyxovirus type 1 (PPMV-1) strains exhibit low virulence in chickens, despite their fusion (F) protein's multi-basic cleavage site. To elucidate the molecular basis of the low pathogenicity of these strains, we constructed an infectious full-length cDNA clone of PPMV-1 strain AV324. This strain is non-virulent for chickens, although its F protein contains the typical virulence motif 112RRKKRF117. By using reverse genetics, we exchanged the F genes of AV324 and a virulent Newcastle disease virus (NDV) strain (Herts) and evaluated the recovered chimeric viruses for their pathogenicity in 1-day-old chickens and in embryonated eggs. Our results show that the F protein of AV324, and probably those of similar PPMV-1 strains, are functionally not different from those of virulent NDV strains and that the difference in pathogenicity must be determined by other factors.
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McClelland, Erin E., Wesley T. Perrine, Wayne K. Potts, and Arturo Casadevall. "Relationship of Virulence Factor Expression to Evolved Virulence in Mouse-Passaged Cryptococcus neoformans Lines." Infection and Immunity 73, no. 10 (October 2005): 7047–50. http://dx.doi.org/10.1128/iai.73.10.7047-7050.2005.
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ABSTRACT Serial passage of Cryptococcus neoformans in mice increases virulence relative to the nonpassaged line. Postpassaged lines showed no difference in the expression of most known virulence factors, with the exception that the more virulent lines had smaller capsules in vitro. These data imply that other mechanisms of virulence remain to be discovered.
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Hoai Thu, Nguyen Thi, Nguyen Thanh Viet, Nghiem Ngoc Minh, and Vo Thi Bich Thuy. "The survey of expression levels of virulent genes in Salmonella strains isolated in retail meats in Hanoi." TAP CHI SINH HOC 40, no. 1 (January 25, 2018): 62–68. http://dx.doi.org/10.15625/0866-7160/v40n1.10633.
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Salmonella is one of the major causes of food poisoning worldwide, especially in developing countries. The virulence of Salmonella is a complex process involving between their virulence factors and the host defenses. The purpose of this study was to detect virulent genes and to assess the level of expression of these genes in five Salmonella strains (including Enteritidis, Albany, Typhimurium, Hadar, and Derby), which were isolated from meat samples at the retail markets in Hanoi. As a result, Salmonella Enteritidis and Salmonella Typhimurium were 100% positive with seven virulent genes, e.g., spiA, spvB, sitC, sifA, sipB, pagC, and invA genes. Salmonella Hadar and Salmonella Derby positive with six genes, except spvB, whereas Salmonella Albany was positive with only the pagC gene. The comparision of the expression levels of these seven virulent genes and the 16S rRNA control gene showed a significantly difference among Salmonella strains (P<0.05). The result of gene expression of seven virulent genes indicate that Salmonella Hadar has the highest gene expression, followed by Salmonella Enteritidis, Salmonella Derby, Salmonella Typhimurium and finally Salmonella Albany. The results of molecular biology analysis will provide additional data on the expression of virulent genes in Salmonella strains isolated from retail meats in Hanoi.
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Oscarsson, Jan, Joseph DiRienzo, and Anders Johansson. "Editorial Comments to the Special Issue: “Aggregatibacter actinomycetemcomitans—Gram-Negative Bacterial Pathogen”." Pathogens 9, no. 6 (June 4, 2020): 441. http://dx.doi.org/10.3390/pathogens9060441.
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Aggregatibacter actinomycetemcomitans is a periodontal pathogen colonizing the oral cavity in many individuals of the human population. It is equipped with several potent virulence factors that can cause cell death and induce or evade the host inflammatory response. Both harmless and highly virulent genotypes of the bacterium have emerged because of the large genetic diversity within the species. The oral condition and age, as well as the geographic origin of the individual, influence the risk to be colonized by a virulent genotype of the bacterium. In the present editorial, the different genetic and virulence properties of A. actinomycetemcomitans will be addressed in relation to the publications in this Special Issue.
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Serrano-Luna, Jesús, Manuel Gutiérrez-Meza, Ricardo Mejía-Zepeda, Silvia Galindo-Gómez, Víctor Tsutsumi, and Mineko Shibayama. "Effect of phosphatidylcholine–cholesterol liposomes on Entamoeba histolytica virulence." Canadian Journal of Microbiology 56, no. 12 (December 2010): 987–95. http://dx.doi.org/10.1139/w10-088.
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Trophozoites of Entamoeba histolytica HM-1:IMSS become less virulent after long-term maintenance in axenic cultures. The factors responsible for the loss of virulence during in vitro cultivation remain unclear. However, it is known that in vitro cultivation of amoeba in culture medium supplemented with cholesterol restores their virulence. In this study, we analyzed the effect of adding phosphatidylcholine–cholesterol (PC–Chol) liposomes to the culture medium and evaluated the effect of this lipid on various biochemical and biological functions of E. histolytica HM-1:IMSS in terms of its virulence. The addition of PC–Chol liposomes to the culture medium maintained the virulence of these parasites against hamster liver at the same level as the original virulent E. histolytica strain, even though these amoebae were maintained without passage through hamster liver for 18 months. The trophozoites also showed increased endocytosis, erythrophagocytosis, and carbohydrate residue expression on the amoebic surface. Protease activities were also modified by the presence of cholesterol in the culture medium. These findings indicate the capacity of cholesterol to preserve amoeba virulence and provide an alternative method for the maintenance of virulent E. histolytica trophozoites without the need for in vivo procedures.
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OLSEN, J. E., T. TIAINEN, and D. J. BROWN. "Levels of virulence are not determined by genomic lineage of Salmonella enterica serotype Enteritidis strains." Epidemiology and Infection 123, no. 3 (December 1999): 423–30. http://dx.doi.org/10.1017/s0950268899003155.
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Mouse virulence and the ability to adhere to, and invade cultured MDCK cells were investigated in 38 phage type reference strains of Salmonella enterica serotype Enteritidis and correlated with genomic lineage. The genomic lineage of 11 of the strains was determined in the present study; one IS200 and one ribotype pattern that had not been reported previously were observed. Log c.f.u. in the spleen 10 days post intraperitoneal (i.p.) infection with 3×103 bacteria (logVC10) varied between 2·9 and 8·7. The reference strains of PT7 and PT23 were found to be semi-rough and were of low virulence. All other strains possessed smooth LPS. Within each of the two major clonal lines, as well as among phage types outside these, both highly virulent and moderate to low virulent strains were present. While all strains of PT1, PT2 and PT8 were highly virulent, low virulent strains were detected in PT4 and PT13. The ability to adhere to, and invade MDCK cells varied between phage types (adherence between 13 and 61% of the inocula and invasion between 4 and 151% of the adherent cells). The results of the cell culture experiments did not correlate with the results of mouse virulence tests. No correlation between clonal lineage and virulence was found within S. Enteritidis. It seems most likely that some strains have lost some of the essential factors enabling this serotype to cause successful systemic infection.
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Sahu, Pramod Kumar, Shailendra Singh, Amrita Gupta, Udai B. Singh, Surinder Paul, Diby Paul, Pandiyan Kuppusamy, Harsh V. Singh, and Anil Kumar Saxena. "A Simplified Protocol for Reversing Phenotypic Conversion of Ralstonia solanacearum during Experimentation." International Journal of Environmental Research and Public Health 17, no. 12 (June 15, 2020): 4274. http://dx.doi.org/10.3390/ijerph17124274.
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Background: Ralstonia solanacearum has the problem of losing the virulence in laboratory conditions, during prolonged experimentation. Since pure colonies of R. solanacearum contain cell fractions differing in virulence, it was considered worthwhile to find a way of selecting the cells with lower attenuation. Therefore, a methodology for inducing virulent-type colonies occurrence in Ralstonia solanacearum was developed. Methods: Nutrient gradient was created by swabbing R. solanacearum culture in a slanted KMTTC medium, and Phyllanthus emblica extract was given by well diffusion. Live–dead cell imaging using BacLight, effects of ascorbic acid on cell viability, and production of virulence factors (exopolysaccharides, cellulase, and pectinase) supported this hypothesis. The tagging of R. solanacearum with green fluorescent protein and further confocal scanning laser microscopic visualization confirmed the colonization in vascular bundles of tomato. Results: P. emblica extract suppressed R. solanacearum initially in well diffusion, but further developed virulent-type colonies around the wells. Nutrient deprivation was found to have synergistic effects with P. emblica extract. The converted fluidal (virulent type) colonies could be able to colonize vascular bundles and cause wilting symptoms. Conclusion: This method will be useful in the laboratories working on biocontrol of R. solanacearum for maintaining virulent-type colonies. Moreover, it could form the basis for studies on the stability of phenotypic conversion and cell fractions in R. solanacearum.
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CHIU, TSAI-HSIN, JINGYUN DUAN, and YI-CHENG SU. "Characteristics of Virulent Vibrio parahaemolyticus Isolated from Oregon and Washington." Journal of Food Protection 70, no. 4 (April 1, 2007): 1011–16. http://dx.doi.org/10.4315/0362-028x-70.4.1011.
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Thirty-four virulent strains of Vibrio parahaemolyticus containing tdh and/or trh genes isolated from Oregon and Washington coastal water were analyzed for O-group antigens and urease activity, and by pulsed-field gel electrophoresis. Six O serotypes (O1, O3, O4, O5, O10, and O11) were identified among the isolates, with the O5 group (19 isolates) being the most prevalent, followed by the O1 group (9 isolates). Nearly all (33 of 34) isolates were capable of producing urease, which reaffirmed the correlation between urease production and virulence factors of V. parahaemolyticus strains isolated from the Pacific Northwest. Pulsed-field gel electrophoresis analysis with NotI and SfiI digestions of the 34 V. parahaemolyticus isolates plus five clinical strains revealed 22 patterns (N1S1 to N20S22), with N1S1 (25.6%) being the most common, followed by N2S2 (10.3%). Nine Oregon isolates were grouped with a 1997 Oregon outbreak strain (027-1C1) with the same serotype (O5), virulence factors (tdh+ and trh+), and genotype (N1S1). Three Washington isolates were found to share the same serotype (O1), virulence factors (tdh+ and trh+), and genotype (N2S2) with a 1997 Washington outbreak strain (10293). The repetitive isolation of virulent strains of V. parahaemolyticus identical to clinical strains involved in previous outbreaks indicates potential hazards associated with oyster consumption. These data may be useful in risk assessment of V. parahaemolyticus infections associated with raw oyster consumption in Oregon and Washington.
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Cooper, Kerry K., Margarethe A. Cooper, Andrea Zuccolo, and Lynn A. Joens. "Re-sequencing of a virulent strain of Campylobacter jejuni NCTC11168 reveals potential virulence factors." Research in Microbiology 164, no. 1 (January 2013): 6–11. http://dx.doi.org/10.1016/j.resmic.2012.10.002.
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Rahman, Mahfuzur, and Zamir K. Punja. "Factors Influencing Development of Root Rot on Ginseng Caused by Cylindrocarpon destructans." Phytopathology® 95, no. 12 (December 2005): 1381–90. http://dx.doi.org/10.1094/phyto-95-1381.
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The fungus Cylindrocarpon destructans (Zins) Scholten is the cause of root rot (disappearing root rot) in many ginseng production areas in Canada. A total of 80 isolates of C. destructans were recovered from diseased roots in a survey of ginseng gardens in British Columbia from 2002-2004. Among these isolates, 49% were classified as highly virulent (causing lesions on unwounded mature roots) and 51% were weakly virulent (causing lesions only on previously wounded roots). Pectinase and polyphenoloxidase enzymes were produced in vitro by C. destructans isolates when they were grown on pectin and phenol as a substrate, respectively. However, highly virulent isolates produced significantly (P < 0.001) higher enzyme levels compared with weakly virulent isolates. Histopathological studies of ginseng roots inoculated with a highly virulent isolate revealed direct hyphal penetration through the epidermis, followed by intracellular hyphal growth in the cortex. Subsequent cell disintegration and accumulation of phenolic compounds was observed. Radial growth of highly and weakly virulent isolates on potato dextrose agar was highest at 18 and 21°C, respectively and there was no growth at 35°C. Mycelial mass production was significantly (P ≤ 0.01) lower at pH 7.0 compared with pH 5.0. To study the effects of pH (5.0 and 7.0) and wounding on disease development, ginseng roots were grown hydroponically in Hoagland's solution. Lesions were significantly larger (P < 0.001) at pH 5.0 compared with pH 7.0 and wounding enhanced disease by a highly virulent isolate at both pHs. In artificially infested soil, 2-year-old ginseng roots were most susceptible to Cylindrocarpon root rot among all root ages tested (1 to 4 years) when evaluated using a combined scale of disease incidence and severity. Root rot severity was significantly (P < 0.002) enhanced by increasing the inoculum density from 3.45 × 102 CFU/g of soil to 1.86 × 103 CFU/g of soil. Disease severity was higher at 20°C compared with 15 and 25°C and at -0.02 MPa soil moisture compared with -0.005 and -0.001 MPa. A significant interaction between soil moisture and temperature was observed for root rot severity.
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Gaspar, Frédéric, Neuza Teixeira, Lionel Rigottier-Gois, Paulo Marujo, Christina Nielsen-LeRoux, Maria Teresa Barreto Crespo, Maria de Fátima Silva Lopes, and Pascale Serror. "Virulence of Enterococcus faecalis dairy strains in an insect model: the role of fsrB and gelE." Microbiology 155, no. 11 (November 1, 2009): 3564–71. http://dx.doi.org/10.1099/mic.0.030775-0.
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Despite the existence of various virulence factors in the Enterococcus genus, enterococcal virulence is still a debated issue. A main consideration is the detection of the same virulence genes in strains isolated from nosocomial or community-acquired infections, and from food products. The goal of this study was to evaluate the roles of two well-characterized enterococcal virulence factors, Fsr and gelatinase, in the potential virulence of Enterococcus faecalis food strains. Virulence of unrelated Enterococcus isolates, including dairy strains carrying fsr and gelE operons, was compared in the Galleria mellonella insect model. E. faecalis dairy strains were able to kill larvae and were as virulent as strain OG1RF, one of the most widely used for virulence studies. In contrast, Enterococcus durans and Enterococcus faecium strains were avirulent or poorly virulent for G. mellonella. To evaluate the role of fsrB and gelE in virulence of E. faecalis dairy strains, both genes were deleted independently in two strains. The ΔfsrB and ΔgelE deletion mutants both produced a gelatinase-negative phenotype. Although both mutations significantly attenuated virulence in G. mellonella, the ΔfsrB strains were more strongly attenuated. These results agree with previous findings suggesting the involvement of fsrB in the control of other cell functions relevant to virulence. Our work demonstrates that the presence of functional fsrB, and to a lesser extent gelE, in dairy enterococci should be considered with caution.
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Gundestrup, Svend, Carsten Struve, Steen G. Stahlhut, and Dennis SchrØder Hansen. "First Case of Liver Abscess in Scandinavia Due to the International Hypervirulent Klebsiella Pneumoniae Clone ST23." Open Microbiology Journal 8, no. 1 (March 7, 2014): 22–24. http://dx.doi.org/10.2174/1874285801408010022.
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This is the first case report from Scandinavia of a pyogenic liver abscess caused by a Klebsiella pneumoniae isolate belonging to the international hyper virulent clone ST23. The patient, an 85-year old Caucasian, had no history of foreign travel or any classical predisposing factors for infection. The isolate was hypermucoviscous of capsular serotype K1 and carried the virulence factors aerobactin, allS, kfu and rmpA.
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Ní Dhufaigh, Kerrie, Natasha Botwright, Eugene Dillon, Ian O’Connor, Eugene MacCarthy, and Orla Slattery. "Differential Exoproteome and Biochemical Characterisation of Neoparamoeba perurans." Microorganisms 9, no. 6 (June 9, 2021): 1258. http://dx.doi.org/10.3390/microorganisms9061258.
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Infection with the protozoan ectoparasite Neoparamoeba perurans, the causative agent of AGD, remains a global threat to salmonid farming. This study aimed to analyse the exoproteome of both an attenuated and virulent N. perurans isolate using proteomics and cytotoxicity testing. A disproportionate presence of proteins from the co-cultured microbiota of N. perurans was revealed on searching an amalgamated database of bacterial, N. perurans and Amoebozoa proteins. LC-MS/MS identified 33 differentially expressed proteins, the majority of which were upregulated in the attenuated exoproteome. Proteins of putative interest found in both exoproteomes were maltoporin, ferrichrome-iron receptor, and putative ferric enterobactin receptor. Protease activity remained significantly elevated in the attenuated exoproteome compared with the virulent exoproteome. Similarly, the attenuated exoproteome had a significantly higher cytotoxic effect on rainbow trout gill cell line (RTgill W1) cells compared with the virulent exoproteome. The presence of a phosphatase and serine protease in the virulent exoproteome may facilitate AGD infection but do not appear to be key players in causing cytotoxicity. Altogether, this study reveals prolonged culture of N. perurans affects the exoproteome composition in favour of nutritional acquisition, and that the current culturing protocol for virulent N. perurans does not facilitate the secretion of virulence factors.
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Gómez-Laguna, Jaime, Fernando Cardoso-Toset, Jazmín Meza-Torres, Javier Pizarro-Cerdá, and Juan J. Quereda. "Virulence potential of Listeria monocytogenes strains recovered from pigs in Spain." Veterinary Record 187, no. 11 (October 6, 2020): e101-e101. http://dx.doi.org/10.1136/vr.105945.
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BackgroundListeria monocytogenes is a foodborne bacterial pathogen that causes listeriosis, an infectious disease in animals and people, with pigs acting as asymptomatic reservoirs. In August 2019 an outbreak associated with the consumption of pork meat caused 222 human cases of listeriosis in Spain. Determining the diversity as well as the virulence potential of strains from pigs is important to public health.MethodsThe behaviour of 23 L monocytogenes strains recovered from pig tonsils, meat and skin was compared by studying (1) internalin A, internalin B, listeriolysin O, actin assembly-inducing protein and PrfA expression levels, and (2) their invasion and intracellular growth in eukaryotic cells.ResultsMarked differences were found in the expression of the selected virulence factors and the invasion and intracellular replication phenotypes of L monocytogenes strains. Strains obtained from meat samples and belonging to serotype 1/2a did not have internalin A anchored to the peptidoglycan. Some strains expressed higher levels of the studied virulence factors and invaded and replicated intracellularly more efficiently than an epidemic L monocytogenes reference strain (F2365).ConclusionThis study demonstrates the presence of virulent L monocytogenes strains with virulent potential in pigs, with valuable implications in veterinary medicine and food safety.
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Sause, William E., Divya Balasubramanian, Irnov Irnov, Richard Copin, Mitchell J. Sullivan, Alexis Sommerfield, Rita Chan, et al. "The purine biosynthesis regulator PurR moonlights as a virulence regulator in Staphylococcus aureus." Proceedings of the National Academy of Sciences 116, no. 27 (June 19, 2019): 13563–72. http://dx.doi.org/10.1073/pnas.1904280116.
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The pathogen Staphylococcus aureus colonizes and infects a variety of different sites within the human body. To adapt to these different environments, S. aureus relies on a complex and finely tuned regulatory network. While some of these networks have been well-elucidated, the functions of more than 50% of the transcriptional regulators in S. aureus remain unexplored. Here, we assess the contribution of the LacI family of metabolic regulators to staphylococcal virulence. We found that inactivating the purine biosynthesis regulator purR resulted in a strain that was acutely virulent in bloodstream infection models in mice and in ex vivo models using primary human neutrophils. Remarkably, these enhanced pathogenic traits are independent of purine biosynthesis, as the purR mutant was still highly virulent in the presence of mutations that disrupt PurR’s canonical role. Through the use of transcriptomics coupled with proteomics, we revealed that a number of virulence factors are differentially regulated in the absence of purR. Indeed, we demonstrate that PurR directly binds to the promoters of genes encoding virulence factors and to master regulators of virulence. These results guided us into further ex vivo and in vivo studies, where we discovered that S. aureus toxins drive the death of human phagocytes and mice, whereas the surface adhesin FnbA contributes to the increased bacterial burden observed in the purR mutant. Thus, S. aureus repurposes a metabolic regulator to directly control the expression of virulence factors, and by doing so, tempers its pathogenesis.
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Bahn, Yong-Sun, Kaihei Kojima, Gary M. Cox, and Joseph Heitman. "Specialization of the HOG Pathway and Its Impact on Differentiation and Virulence ofCryptococcus neoformans." Molecular Biology of the Cell 16, no. 5 (May 2005): 2285–300. http://dx.doi.org/10.1091/mbc.e04-11-0987.
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The human pathogenic fungus Cryptococcus neoformans has diverged from a common ancestor into three biologically distinct varieties or sibling species over the past 10–40 million years. During evolution of these divergent forms, serotype A C. neoformans var. grubii has emerged as the most virulent and cosmopolitan pathogenic clade. Therefore, understanding how serotype A C. neoformans is distinguished from less successful pathogenic serotypes will provide insights into the evolution of fungal virulence. Here we report that the structurally conserved Pbs2-Hog1 MAP kinase cascade has been specifically recruited as a global regulator to control morphological differentiation and virulence factors in the highly virulent serotype A H99 clinical isolate, but not in the laboratory-generated and less virulent serotype D strain JEC21. The mechanisms of Hog1 regulation are strikingly different between the two strains, and the phosphorylation kinetics and localization pattern of Hog1 are opposite in H99 compared with JEC21 and other yeasts. The unique Hog1 regulatory pattern observed in the H99 clinical isolate is widespread in serotype A strains and is also present in some clinical serotype D isolates. Serotype A hog1Δ and pbs2Δ mutants are attenuated in virulence, further underscoring the role of the Pbs2-Hog1 MAPK cascade in the pathogenesis of cryptococcosis.
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Johnson, J. R. "Virulence factors in Escherichia coli urinary tract infection." Clinical Microbiology Reviews 4, no. 1 (January 1991): 80–128. http://dx.doi.org/10.1128/cmr.4.1.80.
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Uropathogenic strains of Escherichia coli are characterized by the expression of distinctive bacterial properties, products, or structures referred to as virulence factors because they help the organism overcome host defenses and colonize or invade the urinary tract. Virulence factors of recognized importance in the pathogenesis of urinary tract infection (UTI) include adhesins (P fimbriae, certain other mannose-resistant adhesins, and type 1 fimbriae), the aerobactin system, hemolysin, K capsule, and resistance to serum killing. This review summarizes the virtual explosion of information regarding the epidemiology, biochemistry, mechanisms of action, and genetic basis of these urovirulence factors that has occurred in the past decade and identifies areas in need of further study. Virulence factor expression is more common among certain genetically related groups of E. coli which constitute virulent clones within the larger E. coli population. In general, the more virulence factors a strain expresses, the more severe an infection it is able to cause. Certain virulence factors specifically favor the development of pyelonephritis, others favor cystitis, and others favor asymptomatic bacteriuria. The currently defined virulence factors clearly contribute to the virulence of wild-type strains but are usually insufficient in themselves to transform an avirulent organism into a pathogen, demonstrating that other as-yet-undefined virulence properties await discovery. Virulence factor testing is a useful epidemiological and research tool but as yet has no defined clinical role. Immunological and biochemical anti-virulence factor interventions are effective in animal models of UTI and hold promise for the prevention of UTI in humans.
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van der Does, H. Charlotte, and Martijn Rep. "Virulence Genes and the Evolution of Host Specificity in Plant-Pathogenic Fungi." Molecular Plant-Microbe Interactions® 20, no. 10 (October 2007): 1175–82. http://dx.doi.org/10.1094/mpmi-20-10-1175.
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In the fungal kingdom, the ability to cause disease in plants appears to have arisen multiple times during evolution. In many cases, the ability to infect particular plant species depends on specific genes that distinguish virulent fungi from their sometimes closely related nonvirulent relatives. These genes encode host-determining “virulence factors,” including small, secreted proteins and enzymes involved in the synthesis of toxins. These virulence factors typically are involved in evolutionary arms races between plants and pathogens. We briefly summarize current knowledge of these virulence factors from several fungal species in terms of function, phylogenetic distribution, sequence variation, and genomic location. Second, we address some issues that are relevant to the evolution of virulence in fungi toward plants; in particular, horizontal gene transfer and the genomic organization of virulence genes.
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ARÉVALO-GALVIS, AZUCENA, ALBA A. TRESPALACIOS-RANGEL, WILLIAM OTERO, MARCELA M. MERCADO-REYES, and RAÚL A. POUTOU-PIÑALES. "Prevalence of cagA, vacA, babA2 and iceA Genes in Helicobacter pylori Strains Isolated from Colombian Patients with Functional Dyspepsia." Polish Journal of Microbiology 61, no. 1 (2012): 33–40. http://dx.doi.org/10.33073/pjm-2012-004.
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The clinical outcome of Helicobacter pylori infection has been particularly associated with virulence genotypes. These genotypes are useful as molecular markers in the identification of patients that are infected and at high risk for developing more severe gastric pathologies. Our main objective was to determine the prevalence of virulence genotypes cagA, vacA, iceA and babA2 of H. pylori, in patients with functional dyspepsia who are infected with the bacteria. H. pylori genotypes babA2 and cagA as well as vacA and iceA allelic variants were identified by PCR in 122 isolates resulting from 79 patients with functional dyspepsia. A high prevalence of genes cagA+ (71%), vacAs1am1 (34%), babA2 (57%) and iceA1 (87%) was found. The most frequent combined genotype found were cagA+/vacAs1am1/babA2+/iceA1 and cagA-/vacAs1am1/babA2+/iceA1, regardless of any family history of gastric cancer or MALT lymphoma. The very virulent genotype cagA+/vacAs1am1/babA2+/iceA1 prevailed in the studied patients with functional dyspepsia. Our results provide information about the prevalence of four of the more important virulent factors and constitute new evidence on the prevalence of the most virulent H. pylori genotype in patients with functional dyspepsia.
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Rajni, Nisha Rao, and Laxman S. Meena. "Biosynthesis and Virulent Behavior of Lipids Produced by Mycobacterium tuberculosis: LAM and Cord Factor: An Overview." Biotechnology Research International 2011 (December 19, 2011): 1–7. http://dx.doi.org/10.4061/2011/274693.
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Mycobacterium tuberculosis is the causative agent of tuberculosis disease, which has developed a myriad of exceptional features contributing to its survival within the hostile environment of host cell. Unique cell wall structure with high lipid content plays an imperative role in the pathogenicity of mycobacteria. Cell wall components of MTB such as lipoarabinomannan and Trehalose dimycolate (cord factor) are virulent in nature apart from its virulence genes. Virulent effect of these factors on host cells reduces host cell immunity. LAM has been known to inhibit phagosome maturation by inhibiting the Ca2+/calmodulin phosphatidyl inositol-3-kinase hvps34 pathways. Moreover, TDM (Trehalose dimycolate) also inhibits fusion between phospholipid vesicles and migration of polymorphonuclear neutrophils. The objective of this paper is to understand the virulence of LAM and cord factor on host cell which might be helpful to design an effective drug against tuberculosis.
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Liu, Yu, Liping Li, Zhiping Luo, Rui Wang, Ting Huang, Wanwen Liang, Qunhong Gu, Fangzhao Yu, and Ming Chen. "Arginine Deiminase and Biotin Metabolism Signaling Pathways Play an Important Role in Human-Derived Serotype V, ST1 Streptococcus agalactiae Virulent Strain upon Infected Tilapia." Animals 10, no. 5 (May 14, 2020): 849. http://dx.doi.org/10.3390/ani10050849.
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Our previous study showed that human-derived Streptococcus agalactiae (serotype V) could infect tilapia, but the mechanism underlying the cross-species infection remains unrecognized. In this study, a multi-omics analysis was performed on human-derived S.agalactiae strain NNA048 (virulent to tilapia, serotype V, ST1) and human-derived S.agalactiae strain NNA038 (non-virulent to tilapia, serotype V, ST1). The results showed that 907 genes (504 up/403 down) and 89 proteins (51 up/38 down) were differentially expressed (p < 0.05) between NNA038 and NNA048. Among them, 56 genes (proteins) were altered with similar trends at both mRNA and protein levels. Functional annotation of them showed that the main differences were enriched in the arginine deiminase system signaling pathway and biotin metabolism signaling pathway: gdhA, glnA, ASL, ADI, OTC, arcC, FabF, FabG, FabZ, BioB and BirA genes may have been important factors leading to the pathogenicity differences between NNA038 and NNA048. We aimed to provide a comprehensive analysis of the human-derived serotype V ST1 S.agalactiae strains, which were virulent and non-virulent to tilapia, and provide a more comprehensive understanding of the virulence mechanism.
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Lan, Shuiyun, Lisa McLay Schelde, Jialong Wang, Naveen Kumar, Hinh Ly, and Yuying Liang. "Development of Infectious Clones for Virulent and Avirulent Pichinde Viruses: a Model Virus To Study Arenavirus-Induced Hemorrhagic Fevers." Journal of Virology 83, no. 13 (April 22, 2009): 6357–62. http://dx.doi.org/10.1128/jvi.00019-09.
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ABSTRACT Several arenaviruses can cause hemorrhagic fever diseases (VHFs) in humans, the pathogenic mechanism of which is poorly understood due to their virulent nature and the lack of molecular clones. A safe, convenient, and economical small animal model of arenavirus hemorrhagic fever is based on guinea pigs infected by the arenavirus Pichinde (PICV). PICV does not cause disease in humans, but an adapted strain of PICV (P18) causes a disease in guinea pigs that mimics arenavirus hemorrhagic fever in humans in many aspects, while a low-passaged strain (P2) remains avirulent in infected animals. In order to identify the virulence determinants within the PICV genome, we developed the molecular clones for both the avirulent P2 and virulent P18 viruses. Recombinant viruses were generated by transfecting plasmids that contain the antigenomic L and S RNA segments of PICV under the control of the T7 promoter into BSRT7-5 cells, which constitutively express T7 RNA polymerase. By analyzing viral growth kinetics in vitro and virulence in vivo, we show that the recombinant viruses accurately recapitulate the replication and virulence natures of their respective parental viruses. Both parental and recombinant virulent viruses led to high levels of viremia and titers in different organs of the infected animals, whereas the avirulent viruses were effectively controlled and cleared by the hosts. These novel infectious clones for the PICV provide essential tools to identify the virulence factors that are responsible for the severe VHF-like disease in infected animals.
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Kłos, Marta, and Jadwiga Wójkowska-Mach. "Pathogenicity of Virulent Species of Group C Streptococci in Human." Canadian Journal of Infectious Diseases and Medical Microbiology 2017 (2017): 1–5. http://dx.doi.org/10.1155/2017/9509604.
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Group C streptococci (GCS) are livestock pathogens and they often cause zoonotic diseases in humans. They are Gram-positive, in mostlyβ-hemolytic and facultative anaerobes. Because of their close evolutionary kinship with group A streptococci (GAS), GCS share many common virulence factors with GAS and cause a similar range of diseases. Due to the exchange of genetic material with GAS, GCS belong to bacteria that are difficult to be distinguished from group A streptococci; GCS are often treated in microbiological diagnostics as contamination of the culture. This report focuses mainly on the pathogenicity of virulent species of GCS and their association with human diseases. The condition that is most frequently quoted is pharyngitis. In this paper, the virulence factors have also been mentioned and an interesting link has been made between GCS and the pathogenesis of rheumatic diseases among the native people of India and Aboriginal populations.
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Lee, Kyung-Woo, and Hyun S. Lillehoj. "Role of Clostridium perfringens Necrotic Enteritis B-like Toxin in Disease Pathogenesis." Vaccines 10, no. 1 (December 31, 2021): 61. http://dx.doi.org/10.3390/vaccines10010061.
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Necrotic enteritis (NE) is a devastating enteric disease caused by Clostridium perfringens type A/G that impacts the global poultry industry by compromising the performance, health, and welfare of chickens. Coccidiosis is a major contributing factor to NE. Although NE pathogenesis was believed to be facilitated by α-toxin, a chromosome-encoded phospholipase C enzyme, recent studies have indicated that NE B-like (NetB) toxin, a plasmid-encoded pore-forming heptameric protein, is the primary virulence factor. Since the discovery of NetB toxin, the occurrence of NetB+ C. perfringens strains has been increasingly reported in NE-afflicted poultry flocks globally. It is generally accepted that NetB toxin is the primary virulent factor in NE pathogenesis although scientific evidence is emerging that suggests other toxins contribute to NE. Because of the complex nature of the host-pathogen interaction in NE pathogenesis, the interaction of NetB with other potential virulent factors of C. perfringens needs better characterization. This short review will summarize the primary virulence factors involved in NE pathogenesis with an emphasis on NetB toxin, and a new detection method for large-scale field screening of NetB toxin in biological samples from NE-afflicted commercial broiler flocks.
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McCool, Logan, Hanh Mai, Michael Essmann, and Bryan Larsen. "Tetracycline Effects onCandida AlbicansVirulence Factors." Infectious Diseases in Obstetrics and Gynecology 2008 (2008): 1–7. http://dx.doi.org/10.1155/2008/493508.
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Object. To determine if tetracycline, previously reported to increase the probability of developing symptomatic vaginal yeast infections, has a direct effect onCandida albicansgrowth or induction of virulent phenotypes.Method. In vitro, clinical isolates of yeast were cultivated with sublethal concentrations of tetracycline and yeast cell counts, hyphal formation, drug efflux pump activity, biofilm production, and hemolysin production were determined by previously reported methods.Results. Tetracycline concentrations above 150 μg/mL inhibitedCandida albicans, but at submicrogram/mL, a modest growth increase during the early hours of the growth curve was observed. Tetracycline did not inhibit hyphal formation at sublethal concentrations. Hypha formation appeared augmented by exposure to tetracycline in the presence of chemically defined medium and especially in the presence of human serum. Efflux pumpCDR1was upregulated and a nonsignificant trend toward increased biofilm formation was noted.Conclusion. Tetracycline appears to have a small growth enhancing effect and may influence virulence through augmentation of hypha formation, and a modest effect on drug efflux and biofilm formation, although tetracycline did not affect hemolysin. It is not clear if the magnitude of the effect is sufficient to attribute vaginitis following tetracycline treatment to direct action of tetracycline on yeast.
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S. El-Kazzaz, Samah, and Noha M. Mahmoud. "Virulence Factors Associated with Quinolone Resistance in Proteus Species Isolated from Patients with Urinary Tract Infection." EJMM-Volume 30-Issue 1 30, no. 1 (January 1, 2021): 115–23. http://dx.doi.org/10.51429/ejmm30115.
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Background: Proteus is an important causative organism of urinary system infections. The invasive nature of Proteus is supported by expression of multiple virulence factors; the infection outcome gets worse when those virulent isolates acquire antibiotic resistant determinants. Objectives: The present study was aiming at isolation of Proteus from urine of patients with urinary tract infections (UTIs) and to assess the relation between virulence factors expression and presence of quinolones resistance genes in those isolates. Methodology: Quinolone resistant Proteus isolates were chosen for detection of quinolone resistance genes, also they were tested for presence of different virulence factors. Results: Sixty eight quinolone resistant Proteus isolates were determined. aac(6′)- Ib-cr was the most frequently detected quinolone resistance gene. Haemagglutination, haemolytic activity, protease production and biofilm formation were documented in 79.4%, 76.5%, 70.6% and 83.8% of the isolates respectively. Conclusion: Proteus isolated from urine displayed many virulence factors and harbored a variety of quinolone resistance genes.
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Picard, Bertrand, José Sevali Garcia, Stéphanie Gouriou, Patrick Duriez, Naïma Brahimi, Edouard Bingen, Jacques Elion, and Erick Denamur. "The Link between Phylogeny and Virulence inEscherichia coli Extraintestinal Infection." Infection and Immunity 67, no. 2 (February 1, 1999): 546–53. http://dx.doi.org/10.1128/iai.67.2.546-553.1999.
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ABSTRACT Previous studies suggesting a link between Escherichia coli phylogenetic groups and extraintestinal virulence have been hampered by the difficulty in establishing the intrinsic virulence of a bacterial strain. Indeed, unidentified virulence factors do exist, and the susceptibility of the host to infection is highly variable. To overcome these difficulties, we have developed a mouse model of extraintestinal virulence to test the virulence of the strains under normalized conditions. We then assessed the phylogenetic relationships compared to the E. coli reference (ECOR) collection, the presence of several known virulence determinants, and the lethality to mice of 82 human adult E. coli strains isolated from normal feces and during the course of extraintestinal infections. Commensal strains belong mainly to phylogenetic groups A and B1, are devoid of virulence determinants, and do not kill the mice. Strains exhibiting the same characteristics as the commensal strains can be isolated under pathogenic conditions, thus indicating the role of host-dependent factors, such as susceptibility linked to underlying disease, in the development of infection. Some strains of phylogenetic groups A, B1, and D are able to kill the mice, their virulence being most often correlated with the presence of virulence determinants. Lastly, strains of the B2 phylogenetic group represent a divergent lineage of highly virulent strains which kill the mice at high frequency and possess the highest level of virulence determinants. The observed link between virulence and phylogeny could correspond to the necessity of virulence determinants in a genetic background that is adequate for the emergence of a virulent clone, an expression of the interdependency of pathogenicity and metabolic activities in pathogenic bacteria.
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HE, YU, SHUAI WANG, XIANTING YIN, FENGJIAO SUN, BIN HE, and XIAO LIU. "Comparison of Extracellular Proteins from Virulent and Avirulent Vibrio parahaemolyticus Strains to Identify Potential Virulence Factors." Journal of Food Protection 83, no. 1 (December 20, 2019): 155–62. http://dx.doi.org/10.4315/0362-028x.jfp-19-188.
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ABSTRACT Vibrio parahaemolyticus is a leading seafood-borne pathogen that causes gastroenteritis, septicemia, and serious wound infections due to the actions of virulence-associated proteins. We compared the extracellular proteins of nonvirulent JHY20 and virulent ATCC 33847 V. parahaemolyticus reference strains. Eighteen extracellular proteins were identified from secretory profiles, and 11 (68.75%) of the 16 proteins in ATCC 33847 are associated with virulence and/or protection against adverse conditions: trigger factor, chaperone SurA, aspartate–semialdehyde dehydrogenase, 4-hydroxy-3-methylbut-2-en-1-yl diphosphate synthase, glutamate 5-kinase, alanine dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase, outer membrane protein OmpV, ribosome-associated inhibitor A, chaperone protein Skp, and universal stress protein. Two nontoxic-related proteins, amino acid ABC transporter substrate-binding protein and an uncharacterized protein, were identified in JHY20. The results provide a theoretical basis for supporting safety risk assessment of aquatic foods, illuminate the pathogenic mechanisms of V. parahaemolyticus, and assist the identification of novel vaccine candidates for foodborne pathogens. HIGHLIGHTS
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Keller, Ninette, Linda S. Jacobson, Mirinda Nel, Marizelle Clerq, Peter N. Thompson, and Johan P. Schoeman. "Prevalence and Risk Factors of Hypoglycemia in Virulent Canine Babesiosis." Journal of Veterinary Internal Medicine 18, no. 3 (May 2004): 265–70. http://dx.doi.org/10.1111/j.1939-1676.2004.tb02544.x.
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Chaiden, Chadaporn, Janthima Jaresitthikunchai, Narumon Phaonakrop, Sittiruk Roytrakul, Anusak Kerdsin, and Suphachai Nuanualsuwan. "Peptidomics Analysis of Virulent Peptides Involved in Streptococcus suis Pathogenesis." Animals 11, no. 9 (August 24, 2021): 2480. http://dx.doi.org/10.3390/ani11092480.
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Streptococcus suis (S. suis) is a zoonotic pathogen causing severe streptococcal disease worldwide. S. suis infections in pigs and humans are frequently associated with the virulent S. suis serotype 2 (SS2). Though various virulence factors of S. suis have been proposed, most of them were not essentially accounted for in the experimental infections. In the present study, we compared the peptidomes of highly virulent SS2 and SS14 in humans, the swine causative serotypes SS7 and SS9, and the rarely reported serotypes SS25 and SS27, and they were cultured in a specified culture medium containing whole blood to simulate their natural host environment. LC-MS/MS could identify 22 unique peptides expressed in the six S. suis serotypes. Under the host-simulated environment, peptides from the ABC-type phosphate transport system (SSU05_1106) and 30S ribosomal protein S2 (rpsB) were detected in the peptidome of virulent SS2 and SS14. Therefore, we suggest that these two proteins or their derived peptides might be involved in the survival of S. suis when simulated with a blood environment.
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Casaz, Paul, Lynne K. Garrity-Ryan, David McKenney, Caroline Jackson, Stuart B. Levy, S. Ken Tanaka, and Michael N. Alekshun. "MarA, SoxS and Rob function as virulence factors in an Escherichia coli murine model of ascending pyelonephritis." Microbiology 152, no. 12 (December 1, 2006): 3643–50. http://dx.doi.org/10.1099/mic.0.2006/000604-0.
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MarA, SoxS and Rob are transcription factors belonging to the AraC family. While these proteins have been associated historically with control of multiple antibiotic resistance, and tolerance to oxidative stress agents and organic solvents, only a paucity of experimental data support a role in regulating virulence. Clinical Escherichia coli isolates, and isogenic strains lacking marA, soxS and rob, were studied in a murine model of ascending pyelonephritis, which is a clinically relevant model of urinary tract infection. Organisms lacking all three transcription factors (triple knockouts) were significantly less virulent than parental strains, and complementation studies demonstrated that the addition of marA, soxS and rob individually restored wild-type virulence in the triple-knockout strain. Deletion of soxS or rob alone was more detrimental than the removal of marA. Thus, all three proteins contribute to virulence in vivo.
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BOREK, ANNA L., JOANNA WILEMSKA, RADOSŁAW IZDEBSKI, WALERIA HRYNIEWICZ, and IZABELA SITKIEWICZ. "A New Rapid and Cost-Effective Method for Detection of Phages, ICEs and Virulence Factors Encoded by Streptococcus pyogenes." Polish Journal of Microbiology 60, no. 3 (2011): 187–201. http://dx.doi.org/10.33073/pjm-2011-027.
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Streptococcus pyogenes (group A Streptococcus, GAS) is a human pathogen that causes diseases of various intensity, from mild strep throat to life threatening invasive infections and postinfectional sequelae. S. pyogenes encodes multiple, often phage encoded, virulence factors and their presence is related to severity of the disease. Acquisition of mobile genetic elements, carrying virulence factors, as phages or ICEs (integrative and cojugative elements) has been shown previously to promote selection of virulent clones. We designed the system of eight low volume multi- and one singleplex PCR reactions to detect genes encoding twenty virulence factors (spd3, sdc, sdaB, sdaD, speB, spyCEP, scpA, mac, sic, speL, K, M, C, I, A, H, G, J, smeZ and ssa) and twenty one phage and ICE integration sites described so far for S. pyogenes. Classification of strains based on the phage and virulence factors absence or presence, correlates with PFGE MLST and emm typing results. We developed a novel, fast and cost effective system that can be used to detect GAS virulence factors. Moreover, this system may become an alternative and effective system to differentiate between GAS strains.
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Spidlova, Petra, Pavla Stojkova, Anders Sjöstedt, and Jiri Stulik. "Control of Francisella tularensis Virulence at Gene Level: Network of Transcription Factors." Microorganisms 8, no. 10 (October 21, 2020): 1622. http://dx.doi.org/10.3390/microorganisms8101622.
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Regulation of gene transcription is the initial step in the complex process that controls gene expression within bacteria. Transcriptional control involves the joint effort of RNA polymerases and numerous other regulatory factors. Whether global or local, positive or negative, regulators play an essential role in the bacterial cell. For instance, some regulators specifically modify the transcription of virulence genes, thereby being indispensable to pathogenic bacteria. Here, we provide a comprehensive overview of important transcription factors and DNA-binding proteins described for the virulent bacterium Francisella tularensis, the causative agent of tularemia. This is an unexplored research area, and the poorly described networks of transcription factors merit additional experimental studies to help elucidate the molecular mechanisms of pathogenesis in this bacterium, and how they contribute to disease.
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Turbyfill, K. Ross, Antoinette B. Hartman, and Edwin V. Oaks. "Isolation and Characterization of a Shigella flexneri Invasin Complex Subunit Vaccine." Infection and Immunity 68, no. 12 (December 1, 2000): 6624–32. http://dx.doi.org/10.1128/iai.68.12.6624-6632.2000.
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ABSTRACT The invasiveness and virulence of Shigella spp. are largely due to the expression of plasmid-encoded virulence factors, among which are the invasion plasmid antigens (Ipa proteins). After infection, the host immune response is directed primarily against lipopolysaccharide (LPS) and the virulence proteins (IpaB, IpaC, and IpaD). Recent observations have indicated that the Ipa proteins (IpaB, IpaC, and possibly IpaD) form a multiprotein complex capable of inducing the phagocytic event which internalizes the bacterium. We have isolated a complex of invasins and LPS from water-extractable antigens of virulent shigellae by ion-exchange chromatography. Western blot analysis of the complex indicates that all of the major virulence antigens of Shigella, including IpaB, IpaC, and IpaD, and LPS are components of this macromolecular complex. Mice or guinea pigs immunized intranasally with purified invasin complex (invaplex), without any additional adjuvant, mounted a significant immunoglobulin G (IgG) and IgA antibody response against theShigella virulence antigens and LPS. The virulence-specific response was very similar to that previously noted in primates infected with shigellae. Guinea pigs (keratoconjunctivitis model) or mice (lethal lung model) immunized intranasally on days 0, 14, and 28 and challenged 3 weeks later with virulent shigellae were protected from disease (P < 0.01 for both animal models).