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1
Allen, Jonathan P., Egon A. Ozer, George Minasov, Ludmilla Shuvalova, Olga Kiryukhina, Wayne F. Anderson, Karla J. F. Satchell e Alan R. Hauser. "A comparative genomics approach identifies contact-dependent growth inhibition as a virulence determinant". Proceedings of the National Academy of Sciences 117, n. 12 (10 marzo 2020): 6811–21. http://dx.doi.org/10.1073/pnas.1919198117.
Abstract (sommario):
Emerging evidence suggests thePseudomonas aeruginosaaccessory genome is enriched with uncharacterized virulence genes. Identification and characterization of such genes may reveal novel pathogenic mechanisms used by particularly virulent isolates. Here, we utilized a mouse bacteremia model to quantify the virulence of 100 individualP. aeruginosabloodstream isolates and performed whole-genome sequencing to identify accessory genomic elements correlated with increased bacterial virulence. From this work, we identified a specific contact-dependent growth inhibition (CDI) system enriched among highly virulentP. aeruginosaisolates. CDI systems contain a large exoprotein (CdiA) with a C-terminal toxin (CT) domain that can vary between different isolates within a species. Prior work has revealed that delivery of a CdiA-CT domain upon direct cell-to-cell contact can inhibit replication of a susceptible target bacterium. Aside from mediating interbacterial competition, we observed our virulence-associated CdiA-CT domain to promote toxicity against mammalian cells in culture and lethality during mouse bacteremia. Structural and functional studies revealed this CdiA-CT domain to have in vitro tRNase activity, and mutations that abrogated this tRNAse activity in vitro also attenuated virulence. Furthermore, CdiA contributed to virulence in mice even in the absence of contact-dependent signaling. Overall, our findings indicate that thisP. aeruginosaCDI system functions as both an interbacterial inhibition system and a bacterial virulence factor against a mammalian host. These findings provide an impetus for continued studies into the complex role of CDI systems inP. aeruginosapathogenesis.
2
Cooper, T. F., e J. A. Heinemann. "Selection for plasmid post–segregational killing depends on multiple infection: evidence for the selection of more virulent parasites through parasite–level competition". Proceedings of the Royal Society B: Biological Sciences 272, n. 1561 (22 febbraio 2005): 403–10. http://dx.doi.org/10.1098/rspb.2004.2921.
Abstract (sommario):
Is the virulence of parasites an outcome of optimized infection? Virulence has often been considered an inevitable consequence of parasite reproduction when the cost incurred by the parasite in reducing the fitness of its current host is offset by increased infection of new hosts. More recent models have focused on how competition occurring between parasites during co–infection might effect selection of virulence. For example, if co–infection was common, parasites with higher intrinsic growth rates might be selected, even at the expense of being optimally adapted to infect new hosts. If growth rate is positively correlated with virulence, then competition would select increased virulence. We tested these models using a plasmid–encoded virulence determinant. The virulence determinant did not contribute to the plasmid's reproduction within or between hosts. Despite this, virulent plasmids were more successful than avirulent derivatives during selection in an environment allowing within–host competition. To explain these findings we propose and test a model in which virulent parasites are selected by reducing the reproduction of competitors.
3
Enkerli, Jürg, Garima Bhatt e Sarah F. Covert. "Maackiain Detoxification Contributes to the Virulence of Nectria haematococca MP VI on Chickpea". Molecular Plant-Microbe Interactions® 11, n. 4 (aprile 1998): 317–26. http://dx.doi.org/10.1094/mpmi.1998.11.4.317.
Abstract (sommario):
Nectria haematococca mating population (MP) VI isolates that contain the MAK1 gene are able to degrade maackiain, a chickpea (Cicer arietinum) phytoalexin, to a less toxic compound. To test the contribution of MAK1 to the virulence of N. haematococca MP VI on chickpea, the MAK1 gene was disrupted in a highly virulent Mak+ isolate or added to a weakly virulent Mak- isolate via transformation. The disruption of MAK1 decreased virulence to a moderate level, while addition of multiple copies of MAK1 increased virulence to either a moderate or a high level. These data demonstrate that maackiain detoxification is a determinant, but not the only determinant, of virulence in N. haematococca MP VI isolates capable of causing disease on chickpea. MAK1 is located on a 1.6-Mb conditionally dispensable chromosome. To ascertain if there are additional genes influencing virulence toward chickpea stems on the MAK1 chromosome, the loss of this chromosome was chemically induced in an isolate containing the disrupted MAK1 gene. Loss of the MAK1 chromosome did not reduce virulence toward chickpea stems further, thus indicating that no additional genes for virulence on this part of the host plant are located on the MAK1 chromosome.
4
Sanz-Ramos, Marta, Fayna Díaz-San Segundo, Cristina Escarmís, Esteban Domingo e Noemí Sevilla. "Hidden Virulence Determinants in a Viral Quasispecies In Vivo". Journal of Virology 82, n. 21 (20 agosto 2008): 10465–76. http://dx.doi.org/10.1128/jvi.00825-08.
Abstract (sommario):
ABSTRACT The characterization of virulence determinants of pathogenic agents is of utmost relevance for the design of disease control strategies. So far, two classes of virulence determinants have been characterized for viral populations: those imprinted in the nucleotide sequence of some specific genomic regions and those that depend on the complexity of the viral population as such. Here we provide evidence of a virulence determinant that depends neither on a genomic sequence nor on detectable differences in population complexity. Foot-and-mouth disease virus is lethal for C57BL/6 mice showing the highest viral load in pancreas. Virus isolated from pancreas after one passage in mice showed an attenuated phenotype, with no lethality even at the highest dose tested. By contrast, virus from sera of the same mice displayed a virulence similar to that of the parental wild-type clone and virus isolated from spleen displayed an intermediate phenotype. However, viral populations from pancreas, spleen, and serum showed indistinguishable consensus genomic nucleotide sequences and mutant spectrum complexities, as quantified according to the mutation frequencies of both entire genomic nucleotide sequences of biological clones. The results show that the populations with differing virulences cannot be distinguished either by the consensus sequence or by the average complexity of the mutant spectrum. Differential harvesting of virus generated by cell transfection of RNA from serum and pancreas failed to reveal genetic differences between subpopulations endowed with differing virulences. In addition to providing evidence of hidden virulence determinants, this study underlines the capacity of a clone of an RNA virus to rapidly diversify phenotypically in vivo.
5
Montes, Nuria, Alberto Cobos, Miriam Gil-Valle, Elena Caro e Israel Pagán. "Arabidopsis thaliana Genes Associated with Cucumber mosaic virus Virulence and Their Link to Virus Seed Transmission". Microorganisms 9, n. 4 (27 marzo 2021): 692. http://dx.doi.org/10.3390/microorganisms9040692.
Abstract (sommario):
Virulence, the effect of pathogen infection on progeny production, is a major determinant of host and pathogen fitness as it affects host fecundity and pathogen transmission. In plant–virus interactions, ample evidence indicates that virulence is genetically controlled by both partners. However, the host genetic determinants are poorly understood. Through a genome-wide association study (GWAS) of 154 Arabidopsis thaliana genotypes infected by Cucumber mosaic virus (CMV), we identified eight host genes associated with virulence, most of them involved in response to biotic stresses and in cell wall biogenesis in plant reproductive structures. Given that virulence is a main determinant of the efficiency of plant virus seed transmission, we explored the link between this trait and the genetic regulation of virulence. Our results suggest that the same functions that control virulence are also important for CMV transmission through seeds. In sum, this work provides evidence of a novel role for some previously known plant defense genes and for the cell wall metabolism in plant virus interactions.
6
MIKI, Tsuyoshi. "Virulence determinant of Chromobacterium violaceum". Nippon Saikingaku Zasshi 69, n. 4 (2014): 577–88. http://dx.doi.org/10.3412/jsb.69.577.
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Zhu, Yefei, Renu Nandakumar, Marat R. Sadykov, Nandakumar Madayiputhiya, Thanh T. Luong, Rosmarie Gaupp, Chia Y. Lee e Greg A. Somerville. "RpiR Homologues May Link Staphylococcus aureus RNAIII Synthesis and Pentose Phosphate Pathway Regulation". Journal of Bacteriology 193, n. 22 (16 settembre 2011): 6187–96. http://dx.doi.org/10.1128/jb.05930-11.
Abstract (sommario):
Staphylococcus aureusis a medically important pathogen that synthesizes a wide range of virulence determinants. The synthesis of many staphylococcal virulence determinants is regulated in part by stress-induced changes in the activity of the tricarboxylic acid (TCA) cycle. One metabolic change associated with TCA cycle stress is an increased concentration of ribose, leading us to hypothesize that a pentose phosphate pathway (PPP)-responsive regulator mediates some of the TCA cycle-dependent regulatory effects. Using bioinformatics, we identified three potential ribose-responsive regulators that belong to the RpiR family of transcriptional regulators. To determine whether these RpiR homologues affect PPP activity and virulence determinant synthesis, therpiRhomologues were inactivated, and the effects on PPP activity and virulence factor synthesis were assessed. Two of the three homologues (RpiRB and RpiRC) positively influence the transcription of the PPP genesrpiAandzwf, while the third homologue (RpiRA) is slightly antagonistic to the other homologues. In addition, inactivation of RpiRC altered the temporal transcription of RNAIII, the effector molecule of theagrquorum-sensing system. These data confirm the close linkage of central metabolism and virulence determinant synthesis, and they establish a metabolic override for quorum-sensing-dependent regulation of RNAIII transcription.
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Neilan, J. G., L. Zsak, Z. Lu, G. F. Kutish, C. L. Afonso e D. L. Rock. "Novel Swine Virulence Determinant in the Left Variable Region of the African Swine Fever Virus Genome". Journal of Virology 76, n. 7 (1 aprile 2002): 3095–104. http://dx.doi.org/10.1128/jvi.76.7.3095-3104.2002.
Abstract (sommario):
ABSTRACT Previously we have shown that the African swine fever virus (ASFV) NL gene deletion mutant E70ΔNL is attenuated in pigs. Our recent observations that NL gene deletion mutants of two additional pathogenic ASFV isolates, Malawi Lil-20/1 and Pr4, remained highly virulent in swine (100% mortality) suggested that these isolates encoded an additional virulence determinant(s) that was absent from E70. To map this putative virulence determinant, in vivo marker rescue experiments were performed by inoculating swine with infection-transfection lysates containing E70 NL deletion mutant virus (E70ΔNL) and cosmid DNA clones from the Malawi NL gene deletion mutant (MalΔNL). A cosmid clone representing the left-hand 38-kb region (map units 0.05 to 0.26) of the MalΔNL genome was capable of restoring full virulence to E70ΔNL. Southern blot analysis of recovered virulent viruses confirmed that they were recombinant E70ΔNL genomes containing a 23- to 28-kb DNA fragment of the Malawi genome. These recombinants exhibited an unaltered MalΔNL disease and virulence phenotype when inoculated into swine. Additional in vivo marker rescue experiments identified a 20-kb fragment, encoding members of multigene families (MGF) 360 and 530, as being capable of fully restoring virulence to E70ΔNL. Comparative nucleotide sequence analysis of the left variable region of the E70ΔNL and Malawi Lil-20/1 genomes identified an 8-kb deletion in the E70ΔNL isolate which resulted in the deletion and/or truncation of three MGF 360 genes and four MGF 530 genes. A recombinant MalΔNL deletion mutant lacking three members of each MGF gene family was constructed and evaluated for virulence in swine. The mutant virus replicated normally in macrophage cell culture but was avirulent in swine. Together, these results indicate that a region within the left variable region of the ASFV genome containing the MGF 360 and 530 genes represents a previously unrecognized virulence determinant for domestic swine.
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Gaupp, Rosmarie, Jessica Wirf, B. Wonnenberg, Tanja Biegel, J. Eisenbeis, J. Graham, M. Herrmann et al. "RpiRc Is a Pleiotropic Effector of Virulence Determinant Synthesis and Attenuates Pathogenicity in Staphylococcus aureus". Infection and Immunity 84, n. 7 (25 aprile 2016): 2031–41. http://dx.doi.org/10.1128/iai.00285-16.
Abstract (sommario):
InStaphylococcus aureus, metabolism is intimately linked with virulence determinant biosynthesis, and several metabolite-responsive regulators have been reported to mediate this linkage.S. aureuspossesses at least three members of the RpiR family of transcriptional regulators. Of the three RpiR homologs, RpiRc is a potential regulator of the pentose phosphate pathway, which also regulates RNAIII levels. RNAIII is the regulatory RNA of theagrquorum-sensing system that controls virulence determinant synthesis. The effect of RpiRc on RNAIII likely involves other regulators, as the regulators that bind the RNAIII promoter have been intensely studied. To determine which regulators might bridge the gap between RpiRc and RNAIII,sarA,sigB,mgrA, andacnAmutations were introduced into anrpiRcmutant background, and the effects on RNAIII were determined. Additionally, phenotypic and genotypic differences were examined in the single and double mutant strains, and the virulence of select strains was examined using two different murine infection models. The data suggest that RpiRc affects RNAIII transcription and the synthesis of virulence determinants in concert with σB, SarA, and the bacterial metabolic status to negatively affect virulence.
10
Kielian, Tammy, Ambrose Cheung e William F. Hickey. "Diminished Virulence of an Alpha-Toxin Mutant ofStaphylococcus aureus in Experimental Brain Abscesses". Infection and Immunity 69, n. 11 (1 novembre 2001): 6902–11. http://dx.doi.org/10.1128/iai.69.11.6902-6911.2001.
Abstract (sommario):
ABSTRACT Staphylococcus aureus is one of the major etiologic agents of brain abscesses in humans, occasionally leading to focal neurological deficits and even death. The objective of the present study was to identify key virulence determinants contributing to the pathogenesis of S. aureus in the brain using a murine brain abscess model. The importance of virulence factor production in disease development was demonstrated by the inability of heat-inactivated S. aureus to induce proinflammatory cytokine or chemokine expression or brain abscess formation in vivo. To directly address the contribution of virulence determinants in brain abscess development, the abilities of S. aureus strains with mutations in the global regulatory loci sarA andagr were examined. An S. aureus sarA agr double mutant exhibited reduced virulence in vivo, as demonstrated by attenuated proinflammatory cytokine and chemokine expression and bacterial replication. Subsequent studies focused on the expression of factors that are altered in thesarA agr double mutant. Evaluation of an alpha-toxin mutant revealed a phenotype similar to that of the sarA agr mutant in vivo, as evidenced by lower bacterial burdens and attenuation of cytokine and chemokine expression in the brain. This suggested that alpha-toxin is a central virulence determinant in brain abscess development. Another virulence mechanism utilized by staphylococci is intracellular survival. Cells recovered from brain abscesses were shown to harbor S. aureusintracellularly, providing a means by which the organism may establish chronic infections in the brain. Together, these data identify alpha-toxin as a key virulence determinant for the survival ofS. aureus in the brain.
11
Kanno, Toru, David Mackay, Toru Inoue, Ginette Wilsden, Makoto Yamakawa, Reiko Yamazoe, Shigeo Yamaguchi, Junsuke Shirai, Paul Kitching e Yosuke Murakami. "Mapping the Genetic Determinants of Pathogenicity and Plaque Phenotype in Swine Vesicular Disease Virus". Journal of Virology 73, n. 4 (1 aprile 1999): 2710–16. http://dx.doi.org/10.1128/jvi.73.4.2710-2716.1999.
Abstract (sommario):
ABSTRACT A series of recombinant viruses were constructed using infectious cDNA clones of the virulent J1’73 (large plaque phenotype) and the avirulent H/3’76 (small plaque phenotype) strains of swine vesicular disease virus to identify the genetic determinants of pathogenicity and plaque phenotype. Both traits could be mapped to the region between nucleotides (nt) 2233 and 3368 corresponding to the C terminus of VP3, the whole of VP1, and the N terminus of 2A. In this region, there are eight nucleotide differences leading to amino acid changes between the J1’73 and the H/3’76 strains. Site-directed mutagenesis of individual nucleotides from the virulent to the avirulent genotype and vice versa indicated that A at nt 2832, encoding glycine at VP1-132, and G at nt 3355, encoding arginine at 2APRO-20, correlated with a large-plaque phenotype and virulence in pigs, irrespective of the origin of the remainder of the genome. Of these two sites, 2APRO-20 appeared to be the dominant determinant for the large-plaque phenotype but further studies are required to elucidate their relative importance for virulence in pigs.
12
Peacock, Sharon J., Catrin E. Moore, Anita Justice, Maria Kantzanou, Lisa Story, Kathryn Mackie, Gael O'Neill e Nicholas P. J. Day. "Virulent Combinations of Adhesin and Toxin Genes in Natural Populations of Staphylococcus aureus". Infection and Immunity 70, n. 9 (settembre 2002): 4987–96. http://dx.doi.org/10.1128/iai.70.9.4987-4996.2002.
Abstract (sommario):
ABSTRACT Most cases of severe Staphylococcus aureus disease cannot be explained by the action of a single virulence determinant, and it is likely that a number of factors act in combination during the infective process. This study examined the relationship between disease in humans and a large number of putative virulence determinants, both individually and in combination. S. aureus isolates (n = 334) from healthy blood donors and from patients with invasive disease were compared for variation in the presence of 33 putative virulence determinants. After adjusting for the effect of clonality, seven determinants (fnbA, cna, sdrE, sej, eta, hlg, and ica) were significantly more common in invasive isolates. All seven factors contributed independently to virulence. No single factor predominated as the major predictor of virulence, their effects appearing to be cumulative. No combinations of the seven genes were either more or less likely to cause disease than others with the same number of virulence-associated genes. There was evidence of considerable horizontal transfer of genes on a background of clonality. Our findings also suggested that allelic variants of a polymorphic locus can make different contributions to the disease process, further study of which is likely to expand our understanding of staphylococcal disease pathogenesis.
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Somerville, Greg A., e Richard A. Proctor. "At the Crossroads of Bacterial Metabolism and Virulence Factor Synthesis in Staphylococci". Microbiology and Molecular Biology Reviews 73, n. 2 (giugno 2009): 233–48. http://dx.doi.org/10.1128/mmbr.00005-09.
Abstract (sommario):
SUMMARY Bacteria live in environments that are subject to rapid changes in the availability of the nutrients that are necessary to provide energy and biosynthetic intermediates for the synthesis of macromolecules. Consequently, bacterial survival depends on the ability of bacteria to regulate the expression of genes coding for enzymes required for growth in the altered environment. In pathogenic bacteria, adaptation to an altered environment often includes activating the transcription of virulence genes; hence, many virulence genes are regulated by environmental and nutritional signals. Consistent with this observation, the regulation of most, if not all, virulence determinants in staphylococci is mediated by environmental and nutritional signals. Some of these external signals can be directly transduced into a regulatory response by two-component regulators such as SrrAB; however, other external signals require transduction into intracellular signals. Many of the external environmental and nutritional signals that regulate virulence determinant expression can also alter bacterial metabolic status (e.g., iron limitation). Altering the metabolic status results in the transduction of external signals into intracellular metabolic signals that can be “sensed” by regulatory proteins (e.g., CodY, Rex, and GlnR). This review uses information derived primarily using Bacillus subtilis and Escherichia coli to articulate how gram-positive pathogens, with emphasis on Staphylococcus aureus and Staphylococcus epidermidis, regulate virulence determinant expression in response to a changing environment.
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Rout, Subrat N., e Siba K. Samal. "The Large Polymerase Protein Is Associated with the Virulence of Newcastle Disease Virus". Journal of Virology 82, n. 16 (11 giugno 2008): 7828–36. http://dx.doi.org/10.1128/jvi.00578-08.
Abstract (sommario):
ABSTRACT Naturally occurring Newcastle disease virus (NDV) strains vary greatly in virulence, ranging from no apparent infection to severe disease causing 100% mortality in chickens. The viral determinants of NDV virulence are not completely understood. Cleavage of the fusion protein is required for the initiation of infection, and it acts as a determinant of virulence. The attachment protein HN was found to play a minor role in virulence. In this study, we have evaluated the role of the internal proteins (N, P, and L) in NDV virulence by using a chimeric reverse-genetics approach. The N, P, and L genes were exchanged individually between an avirulent NDV strain, LaSota, and an intermediate virulent NDV strain, Beaudette C (BC), and the N and P genes were also exchanged together. The recovered chimeric viruses were evaluated for their pathogenicity in the natural host, chickens. Our results showed that the pathogenicities of N and P chimeric viruses were similar to those of their respective parental viruses, indicating that the N and P genes probably play minor roles in virulence. However, replacement of the L gene of BC with that of LaSota significantly increased the pathogenicity of the L-chimeric virus, suggesting that the L gene probably contributes to the virulence of NDV. The L-chimeric BC virus was found to replicate at a 100-fold-higher level than its parental virus in chicken brain, suggesting that the increase in pathogenicity may be due to the increased replication level of the chimeric virus. Our findings offer new insights into the pathogenesis of NDV infection.
15
Zhan, Binhui, Wenyang Zhao, Shifang Li, Xiuling Yang e Xueping Zhou. "Functional Scanning of Apple Geminivirus Proteins as Symptom Determinants and Suppressors of Posttranscriptional Gene Silencing". Viruses 10, n. 9 (11 settembre 2018): 488. http://dx.doi.org/10.3390/v10090488.
Abstract (sommario):
Apple geminivirus (AGV) is a recently identified geminivirus which is isolated from the apple tree in China. We carried out functional scanning of apple geminivirus proteins as symptom determinants and suppressors of posttranscriptional gene silencing (PTGS). Our results indicated that AGV V2 is an important virulence factor localized to the nucleus and cytoplasm that suppresses PTGS and induces severe symptoms of crinkling and necrosis. AGV C1 is also a virulence determinant which elicits systemic necrosis when expressed from a PVX-based vector. The AGV C4 is targeted to cytoplasm, plasma membrane, nucleus, and chloroplasts. The inoculation of PVX-C4 on N. benthamiana induced severe upward leaf curling, which implied that AGV C4 also functions as a symptom determinant, and mutation analyses suggested that the acylated residues on Gly2 and Cys8 play important roles in its subcellular localization and symptom development.
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MacFarlane, Ryan C., e Upinder Singh. "Identification of an Entamoeba histolytica Serine-, Threonine-, and Isoleucine-Rich Protein with Roles in Adhesion and Cytotoxicity". Eukaryotic Cell 6, n. 11 (7 settembre 2007): 2139–46. http://dx.doi.org/10.1128/ec.00174-07.
Abstract (sommario):
ABSTRACT Entamoeba histolytica is a leading cause of parasitic death globally. However, the molecular framework regulating pathogenesis is poorly understood. We have previously used expression profiling to identify Entamoeba genes whose expressions were strictly associated with virulent strains (R. C. MacFarlane and U. Singh, Infect. Immun. 74:340-351, 2006). One gene, which we have named EhSTIRP (Entamoeba histolytica serine-, threonine-, and isoleucine-rich protein), was exclusively expressed in virulent but not in nonvirulent Entamoeba strains. EhSTIRP is predicted to be a transmembrane protein and is encoded by a multigene family. In order to characterize its function in amebic biology, we used a double-stranded RNA-based approach and were able to selectively down-regulate expression of this gene family. Upon EhSTIRP down-regulation, we were able to ascribe cytotoxic and adhesive properties to the protein family using lactate dehydrogenase release and Chinese hamster ovary cell adhesion assays. EhSTIRP thus likely represents a novel determinant of virulence in Entamoeba histolytica. This work validates the fact that genes expressed exclusively in virulent strains may represent virulence determinants and highlights the need for further functional analyses of other genes with similar expression profiles.
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Mascellino, M. T., M. Margani e A. Oliva. "Helicobacter pylori: Determinant and Markers of Virulence". Disease Markers 27, n. 3-4 (2009): 137–56. http://dx.doi.org/10.1155/2009/863493.
Abstract (sommario):
In this review, we examine the main virulence determinants inHelicobacter pylori(Hp) strains and the correlation between these and the different diseases followingHpinfections. We also discuss the host response toHpand the implications and advantages of the development of non-invasive pre-endoscopy screening of molecular and serological markers associated withHpvirulence and disease progression putting an emphasis on new screening techniques such as the Luminex – X multi analytes profiling technology and the multiplex PCR.
18
Chua, K. L., Y. Y. Chan e Y. H. Gan. "Flagella Are Virulence Determinants of Burkholderia pseudomallei". Infection and Immunity 71, n. 4 (aprile 2003): 1622–29. http://dx.doi.org/10.1128/iai.71.4.1622-1629.2003.
Abstract (sommario):
ABSTRACT Burkholderia pseudomallei, a facultatively intracellular pathogen, is a flagellated and motile gram-negative bacterium and is the causative agent of melioidosis in humans. Flagella are commonly recognized as important virulence determinants expressed by bacterial pathogens since the motility phenotype imparted by these organelles often correlates with the ability of an organism to cause disease. We used a virulent isolate of B. pseudomallei, KHW, to construct an isogenic deletion mutant with a mutation in the flagellin gene (fliC) by gene replacement transposon mutagenesis. The KHWΔfliCKm mutant was aflagellate and nonmotile in semisolid agar. The isogenic KHWΔfliCKm mutant was not impaired in terms of the ability to invade and replicate in cultured human lung cells compared with the wild type. It was also equally virulent in slow-killing assays involving Caenorhabditis elegans, but it was avirulent during intranasal infection of BALB/c mice. Very few bacteria, if any, were isolated from the lungs and spleens of KHWΔfliCKm-infected mice. In contrast, the bacterial loads in the lungs and spleens were similar in mice infected with KHW and in mice infected with the complemented mutant, KHWΔfliCKm/pUCP28TfliC. Unlike the Syrian hamster or diabetic rat models of infection, the B. pseudomallei flagellin was also a virulence factor during intraperitoneal infection of BALB/c mice. In this study, all animals infected with KHWΔfliCKm remained healthy and did not succumb to disease regardless of the route of infection. The flagellum is therefore an important and necessary virulence determinant of B. pseudomallei during intranasal and intraperitoneal infection of mice.
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Suthar, Mehul S., Reed Shabman, Kenya Madric, Cassandra Lambeth e Mark T. Heise. "Identification of Adult Mouse Neurovirulence Determinants of the Sindbis Virus Strain AR86". Journal of Virology 79, n. 7 (1 aprile 2005): 4219–28. http://dx.doi.org/10.1128/jvi.79.7.4219-4228.2005.
Abstract (sommario):
ABSTRACT Sindbis virus infection of mice has provided valuable insight into viral and host factors that contribute to virus-induced neurologic disease. In an effort to further define the viral genetic elements that contribute to adult mouse neurovirulence, the neurovirulent Sindbis virus strain AR86 was compared to the closely related (22 single amino acid coding changes and the presence or absence of an 18-amino-acid sequence in nsP3 [positions 386 to 403]) but avirulent Girdwood strain. Initial studies using chimeric viruses demonstrated that genetic elements within the nonstructural and structural coding regions contributed to AR86 neurovirulence. Detailed mapping studies identified three major determinants in the nonstructural region, at nsP1 538 (Ile to Thr; avirulent to virulent), an 18-amino-acid deletion in nsP3 (positions 386 to 403), and nsP3 537 (opal to Cys; avirulent to virulent), as well as a single determinant in the structural genes at E2 243 (Leu to Ser; avirulent to virulent), which were essential for AR86 adult mouse neurovirulence. Replacing these codons in AR86 with those found in Girdwood resulted in the attenuation of AR86, while the four corresponding AR86 changes in the Girdwood genetic background increased virulence to the level of wild-type AR86. The attenuating mutations did not adversely affect viral replication in vitro, and the attenuated viruses established infection in the brain and spinal cord as efficiently as the virulent viruses. However, the virus containing the four virulence determinants grew to higher levels in the spinal cord at late times postinfection, suggesting that the virus containing the four attenuating determinants either failed to spread or was cleared more efficiently than the wild-type virus.
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Pradel, Elizabeth, Nicole Guiso, Franco D. Menozzi e Camille Locht. "Bordetella pertussis TonB, a Bvg-Independent Virulence Determinant". Infection and Immunity 68, n. 4 (1 aprile 2000): 1919–27. http://dx.doi.org/10.1128/iai.68.4.1919-1927.2000.
Abstract (sommario):
ABSTRACT In gram-negative bacteria, high-affinity iron uptake requires the TonB/ExbB/ExbD envelope complex to release iron chelates from their specific outer membrane receptors into the periplasm. Based on sequence similarities, the Bordetella pertussis tonB exbB exbD locus was identified on a cloned DNA fragment. The tight organization of the three genes suggests that they are cotranscribed. A putative Fur-binding sequence located upstream from tonB was detected in a Fur titration assay, indicating that the tonB exbB exbD operon may be Fur-repressed in high-iron growth conditions. Putative structural genes of the β-subunit of the histone-like protein HU and of a new two-component regulatory system were identified upstream from tonB and downstream from exbD, respectively. A B. pertussis ΔtonB exbB::Kmr mutant was constructed by allelic exchange and characterized. The mutant was impaired for growth in low-iron medium in vitro and could not use ferrichrome, desferal, or hemin as iron sources. Levels of production of the major bacterial toxins and adhesins were similar in the TonB+/TonB− pair. The ΔtonB exbBmutant was still responsive to chemical modulators of virulence; thus, the BvgA/BvgS two-component system is not TonB dependent. Nevertheless, in vivo in the mouse respiratory infection model, the colonization ability of the mutant was reduced compared to the parental strain.
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Loutet, Slade A., e Miguel A. Valvano. "A Decade of Burkholderia cenocepacia Virulence Determinant Research". Infection and Immunity 78, n. 10 (19 luglio 2010): 4088–100. http://dx.doi.org/10.1128/iai.00212-10.
Abstract (sommario):
ABSTRACT The Burkholderia cepacia complex (Bcc) is a group of genetically related environmental bacteria that can cause chronic opportunistic infections in patients with cystic fibrosis (CF) and other underlying diseases. These infections are difficult to treat due to the inherent resistance of the bacteria to antibiotics. Bacteria can spread between CF patients through social contact and sometimes cause cepacia syndrome, a fatal pneumonia accompanied by septicemia. Burkholderia cenocepacia has been the focus of attention because initially it was the most common Bcc species isolated from patients with CF in North America and Europe. Today, B. cenocepacia, along with Burkholderia multivorans, is the most prevalent Bcc species in patients with CF. Given the progress that has been made in our understanding of B. cenocepacia over the past decade, we thought that it was an appropriate time to review our knowledge of the pathogenesis of B. cenocepacia, paying particular attention to the characterization of virulence determinants and the new tools that have been developed to study them. A common theme emerging from these studies is that B. cenocepacia establishes chronic infections in immunocompromised patients, which depend more on determinants mediating host niche adaptation than those involved directly in host cells and tissue damage.
22
Murray, Ronan. "Community MRSA and Panton-Valentine leukocidin (PVL): the perfect storm, or a storm in a tea-cup?" Microbiology Australia 29, n. 3 (2008): 143. http://dx.doi.org/10.1071/ma08143.
Abstract (sommario):
Staphylococcus aureus is well known for its propensity to encode and express a formidable range of virulence determinants that can cause considerable morbidity and mortality in its host. Amongst these determinants is Panton-Valentine leukocidin (PVL), a cytolytic exotoxin first described in the late 19th century. This toxin is found in many S. aureus clones; however, of particular concern is the fact that community-acquired methicillin-resistant S. aureus (CA-MRSA) clones that contain the PVL determinant have been associated with severe necrotising cutaneous and pulmonary infections in previously well individuals. These reports raise the spectre of a true ?superbug? ? one that is readily transmissible, resistant to front-line antimicrobial agents, and potentially more virulent that other S. aureus strains. Specific therapeutic approaches directed towards the expression and/or activity of PVL, or the elimination of carriage and transmission of S. aureus that contains PVL determinants, are being considered; however, the effectiveness of such approaches has yet to be determined.
23
Lozano-Mendoza, Janeth, Fátima Ramírez-Montiel, Ángeles Rangel-Serrano, Itzel Páramo-Pérez, Claudia Leticia Mendoza-Macías, Faridi Saavedra-Salazar, Bernardo Franco et al. "Attenuation of In Vitro and In Vivo Virulence Is Associated with Repression of Gene Expression of AIG1 Gene in Entamoeba histolytica". Pathogens 12, n. 3 (21 marzo 2023): 489. http://dx.doi.org/10.3390/pathogens12030489.
Abstract (sommario):
Entamoeba histolytica virulence results from complex host–parasite interactions implicating multiple amoebic components (e.g., Gal/GalNAc lectin, cysteine proteinases, and amoebapores) and host factors (microbiota and immune response). UG10 is a strain derived from E. histolytica virulent HM-1:IMSS strain that has lost its virulence in vitro and in vivo as determined by a decrease of hemolytic, cytopathic, and cytotoxic activities, increased susceptibility to human complement, and its inability to form liver abscesses in hamsters. We compared the transcriptome of nonvirulent UG10 and its parental HM-1:IMSS strain. No differences in gene expression of the classical virulence factors were observed. Genes downregulated in the UG10 trophozoites encode for proteins that belong to small GTPases, such as Rab and AIG1. Several protein-coding genes, including iron-sulfur flavoproteins and heat shock protein 70, were also upregulated in UG10. Overexpression of the EhAIG1 gene (EHI_180390) in nonvirulent UG10 trophozoites resulted in augmented virulence in vitro and in vivo. Cocultivation of HM-1:IMSS with E. coli O55 bacteria cells reduced virulence in vitro, and the EhAIG1 gene expression was downregulated. In contrast, virulence was increased in the monoxenic strain UG10, and the EhAIG1 gene expression was upregulated. Therefore, the EhAIG1 gene (EHI_180390) represents a novel virulence determinant in E. histolytica.
24
Rottier, Peter J. M., Kazuya Nakamura, Pepijn Schellen, Haukeline Volders e Bert Jan Haijema. "Acquisition of Macrophage Tropism during the Pathogenesis of Feline Infectious Peritonitis Is Determined by Mutations in the Feline Coronavirus Spike Protein". Journal of Virology 79, n. 22 (15 novembre 2005): 14122–30. http://dx.doi.org/10.1128/jvi.79.22.14122-14130.2005.
Abstract (sommario):
ABSTRACT In feline coronavirus (FCoV) pathogenesis, the ability to infect macrophages is an essential virulence factor. Whereas the low-virulence feline enteric coronavirus (FECV) isolates primarily replicate in the epithelial cells of the enteric tract, highly virulent feline infectious peritonitis virus (FIPV) isolates have acquired the ability to replicate efficiently in macrophages, which allows rapid dissemination of the virulent virus throughout the body. FIPV 79-1146 and FECV 79-1683 are two genetically closely related representatives of the two pathotypes. Whereas FECV 79-1683 causes at the most a mild enteritis in young kittens, FIPV 79-1146 almost invariably induces a lethal peritonitis. The virulence phenotypes correlate with the abilities of these viruses to infect and replicate in macrophages, a feature of FIPV 79-1146 but not of FECV 79-1683. To identify the genetic determinants of the FIPV 79-1146 macrophage tropism, we exchanged regions of its genome with the corresponding parts of FECV 79-1683, after which the ability of the FIPV/FECV hybrid viruses to infect macrophages was tested. Thus, we established that the FIPV spike protein is the determinant for efficient macrophage infection. Interestingly, this property mapped to the C-terminal domain of the protein, implying that the difference in infection efficiency between the two viruses is not determined at the level of receptor usage, which we confirmed by showing that infection by both viruses was equally blocked by antibodies directed against the feline aminopeptidase N receptor. The implications of these findings are discussed.
25
Lanthier, Martin, Andrew Scott, David R. Lapen, Yun Zhang e Edward Topp. "Frequency of virulence genes and antibiotic resistances inEnterococcusspp. isolates from wastewater and feces of domesticated mammals and birds, and wildlife". Canadian Journal of Microbiology 56, n. 9 (settembre 2010): 715–29. http://dx.doi.org/10.1139/w10-046.
Abstract (sommario):
Enterococci are gastrointestinal tract residents and also an important cause of nosocomial infections. To understand which species, virulence determinants, and antibiotic resistances are prevalent in enterococci shed by various hosts groups, a total of 1460 strains isolated from 144 fecal samples obtained from wastewater, domesticated mammals and birds, and wildlife were characterized. Identification of isolates to the species level showed that Enterococcus faecalis was dominant in domesticated mammals and birds and wildlife feces, whereas Enterococcus faecium was dominant among wastewater isolates, and that no single Enterococcus species could be associated with a specific host group. The frequency of 12 virulence determinants was evaluated among isolates, but no single virulence determinant could be associated with a specific host group. Resistance to 12 antibiotics was evaluated among isolates, and it was shown that the highest frequency of resistance at breakpoint concentration was found in domesticated mammals and birds (P ≤ 0.05 for 4 antibiotics). Our results suggests that (1) species identification and virulence typing of Enterococcus spp. isolates are not useful for the identification of the host groups responsible for fecal contamination of water by microbial source tracking and that (2) antibiotic use for clinical, veterinary, or animal husbandry practices is promoting resistance.
26
Sun, Boguang, Xiao-Hua Zhang, Xuexi Tang, Shushan Wang, Yingbin Zhong, Jixiang Chen e Brian Austin. "A Single Residue Change in Vibrio harveyi Hemolysin Results in the Loss of Phospholipase and Hemolytic Activities and Pathogenicity for Turbot (Scophthalmus maximus)". Journal of Bacteriology 189, n. 6 (12 gennaio 2007): 2575–79. http://dx.doi.org/10.1128/jb.01650-06.
Abstract (sommario):
ABSTRACT Vibrio harveyi hemolysin, an important virulence determinant in fish pathogenesis, was further characterized, and the enzyme was identified as a phospholipase B by gas chromatography. Site-directed mutagenesis revealed that a specific residue, Ser153, was critical for its enzymatic activity and for its virulence in fish.
27
Novik, Veronica, Dirk Hofreuter e Jorge E. Galán. "Characterization of a Campylobacter jejuni VirK Protein Homolog as a Novel Virulence Determinant". Infection and Immunity 77, n. 12 (21 settembre 2009): 5428–36. http://dx.doi.org/10.1128/iai.00528-09.
Abstract (sommario):
ABSTRACT Campylobacter jejuni is a leading cause of food-borne illness in the United States. Despite significant recent advances, its mechanisms of pathogenesis are poorly understood. A unique feature of this pathogen is that, with some exceptions, it lacks homologs of known virulence factors from other pathogens. Through a genetic screen, we have identified a C. jejuni homolog of the VirK family of virulence factors, which is essential for antimicrobial peptide resistance and mouse virulence.
28
Young Lee, Si, John O. Cisar, Joseph L. Bryant, Michael A. Eckhaus e Ann L. Sandberg. "Resistance of Streptococcus gordonii to Polymorphonuclear Leukocyte Killing Is a Potential Virulence Determinant of Infective Endocarditis". Infection and Immunity 74, n. 6 (giugno 2006): 3148–55. http://dx.doi.org/10.1128/iai.00087-06.
Abstract (sommario):
ABSTRACT Significant differences in virulence among seven representative Streptococcus gordonii strains were observed by using the rat model of infective endocarditis. Five strains, including S. gordonii DL1, caused severe disease, while the other two strains, including S. gordonii SK12, caused minimal or no disease. The differences in virulence were evident from the visible presence of streptococci in the vegetations present on the aortic valves of catheterized rats that were challenged with individual strains and also from the much greater recovery of rifampin-resistant S. gordonii DLl than of streptomycin-resistant S. gordonii SK12 from the hearts of animals coinfected with both organisms. Each S. gordonii strain aggregated with human platelets and bound to polymorphonuclear leukocytes (PMNs), as shown by the stimulation of PMN superoxide anion production. These interactions were reduced or abolished by pretreatment of the platelets or PMNs with sialidase, indicating that there was bacterial recognition of host sialic acid-containing receptors. Adhesin-mediated binding of each S. gordonii strain to PMNs also triggered phagocytosis. However, the subsequent PMN-dependent killing differed significantly for the seven strains. The five virulent strains included three strains that were not killed and two strains whose numbers were reduced by approximately 50%. In contrast, the level of killing of each avirulent strain under the same conditions was significantly greater and approached 90% of the bacteria added. Parallel studies performed with rat PMNs revealed comparable differences in the resistance or susceptibility of representative virulent and avirulent strains. Thus, the ability of S. gordonii to survive in PMNs following adhesin-mediated phagocytosis may be an important virulence determinant of infective endocarditis.
29
Bárria, Cátia, Dalila Mil-Homens, Sandra N. Pinto, Arsénio M. Fialho, Cecília M. Arraiano e Susana Domingues. "RNase R, a New Virulence Determinant of Streptococcus pneumoniae". Microorganisms 10, n. 2 (29 gennaio 2022): 317. http://dx.doi.org/10.3390/microorganisms10020317.
Abstract (sommario):
Pneumococcal infections have increasingly high mortality rates despite the availability of vaccines and antibiotics. Therefore, the identification of new virulence determinants and the understanding of the molecular mechanisms behind pathogenesis have become of paramount importance in the search of new targets for drug development. The exoribonuclease RNase R has been involved in virulence in a growing number of pathogens. In this work, we used Galleria mellonella as an infection model to demonstrate that the presence of RNase R increases the pneumococcus virulence. Larvae infected with the RNase R mutant show an increased expression level of antimicrobial peptides. Furthermore, they have a lower bacterial load in the hemolymph in the later stages of infection, leading to a higher survival rate of the larvae. Interestingly, pneumococci expressing RNase R show a sudden drop in bacterial numbers immediately after infection, resembling the eclipse phase observed after intravenous inoculation in mice. Concomitantly, we observed a lower number of mutant bacteria inside larval hemocytes and a higher susceptibility to oxidative stress when compared to the wild type. Together, our results indicate that RNase R is involved in the ability of pneumococci to evade the host immune response, probably by interfering with internalization and/or replication inside the larval hemocytes.
30
Finn, Theresa M., e Lisa A. Stevens. "Tracheal colonization factor: a Bordetella pertussis secreted virulence determinant". Molecular Microbiology 16, n. 4 (maggio 1995): 625–34. http://dx.doi.org/10.1111/j.1365-2958.1995.tb02425.x.
31
Barondess, James J., e Jon Beckwfth. "A bacterial virulence determinant encoded by lysogenic coliphage λ". Nature 346, n. 6287 (agosto 1990): 871–74. http://dx.doi.org/10.1038/346871a0.
32
Chitlaru, Theodor, Galia Zaide, Sharon Ehrlich, Itzhak Inbar, Ofer Cohen e Avigdor Shafferman. "HtrA is a major virulence determinant of Bacillus anthracis". Molecular Microbiology 81, n. 6 (23 agosto 2011): 1542–59. http://dx.doi.org/10.1111/j.1365-2958.2011.07790.x.
33
Peak, Ian R. A., Michael P. Jennings, Derek W. Hood e E. Richard Moxon. "Tetranucleotide repeats identify novel virulence determinant homologues inNeisseria meningitidis". Microbial Pathogenesis 26, n. 1 (gennaio 1999): 13–23. http://dx.doi.org/10.1006/mpat.1998.0243.
34
Way, Sing Sing, e Christopher B. Wilson. "The Mycobacterium tuberculosis ESAT-6 Homologue in Listeria monocytogenes Is Dispensable for Growth In Vitro and In Vivo". Infection and Immunity 73, n. 9 (settembre 2005): 6151–53. http://dx.doi.org/10.1128/iai.73.9.6151-6153.2005.
Abstract (sommario):
ABSTRACT ESAT-6 is a virulence determinant in Mycobacterium tuberculosis and a member of a conserved group of proteins in a variety of other bacteria. A targeted deletion of the homologous gene in Listeria was generated, and in contrast to that observed for mycobacteria, this locus was not required for Listeria virulence.
35
Chavadi, Manjunath, Rahul Narasanna, Ashajyothi Chavan, Ajay Kumar Oli e Chandrakanth Kelmani. R. "Prevalence of Methicillin Resistant and Virulence Determinants in Clinical Isolates of Staphylococcus aureus". Open Infectious Diseases Journal 10, n. 1 (13 agosto 2018): 108–15. http://dx.doi.org/10.2174/1874279301810010108.
Abstract (sommario):
Introduction:Methicillin-resistantStaphylococcus aureus(MRSA) is the major threat that is a result of the uncontrolled use of antibiotics causing a huge loss in health, so understanding their prevalence is necessary as a public health measure.Objective:The aim of this study was to determine the prevalence of methicillin-resistant MRSA and virulence determinant among associatedS. aureusfrom the clinical samples obtained from various hospital and health care centers of the Gulbarga region in India.Materials and Methods:All the collected samples were subjected for the screening ofS. aureusand were further characterized by conventional and molecular methods including their antibiotic profiling. Further, the response of methicillin antibiotic on cell morphology was studied using scanning electron microscopy.Results:A total 126S. aureuswas isolated from the clinical samples which showed, 100% resistant to penicillin, 55.5% to oxacillin, 75.3% to ampicillin, 70.6% to streptomycin, 66.6% to gentamicin, 8.7% to vancomycin and 6.3% to teicoplanin. The selected MRSA strains were found to possessmecA(gene coding for penicillin-binding protein 2A) andfemA(factor essential for methicillin resistance)genetic determinants in their genome with virulence determinants such as Coagulase (coa) and the X region of the protein A (spa)gene. Further, the methicillin response in resistantS. aureusshowed to be enlarged and malformed on cell morphology.Conclusion:The molecular typing of clinical isolates ofS. aureusin this study was highly virulent and also resistant to methicillin; this will assist health professionals to control, exploration of alternative medicines and new approaches to combat Staphylococcal infections more efficiently by using targeted therapy.
36
Byrd, Thomas F., Gary M. Green, Sharon E. Fowlston e C. Rick Lyons. "Differential Growth Characteristics and Streptomycin Susceptibility of Virulent and Avirulent Mycobacterium tuberculosis Strains in a Novel Fibroblast-Mycobacterium Microcolony Assay". Infection and Immunity 66, n. 11 (1 novembre 1998): 5132–39. http://dx.doi.org/10.1128/iai.66.11.5132-5139.1998.
Abstract (sommario):
ABSTRACT The ability to spread from cell to cell may be an important virulence determinant of Mycobacterium tuberculosis. An in vitro assay was developed to characterize this ability among four strains of M. tuberculosis: the attenuated strain H37Ra, the virulent strains H37Rv and Erdman, and a virulent clinical isolate (Stew). Confluent monolayers of human skin fibroblasts were infected with these strains and overlaid with agar-medium. M. tuberculosis infection developed over 21 days as microcolonies originating within the plane of the fibroblasts. Microcolonies of the virulent strains had an elongated appearance and exhibited extensive cording. The cords appeared to invade adjacent cells within the plane of the monolayer. Microcolony diameter of the Erdman strain was significantly larger than that of the other virulent strains, indicating that virulent strains can have distinguishing phenotypes in this assay. In contrast, avirulent H37Ra microcolonies were rounded and noncorded. H37Ra microcolonies were significantly smaller than those of the virulent strains. Microcolony diameter of the virulent strains was not reduced by the extracellularly acting antibiotic streptomycin at concentrations of up to 5.0 μg/ml. In contrast, H37Ra microcolony size was reduced at concentrations as low as 0.5 μg/ml. Growth of all strains was similarly inhibited by 1.0 μg of streptomycin per ml in fibroblast-conditioned tissue culture medium alone. When fibroblasts were infected with the M. tuberculosis strains without an agar overlay, with and without streptomycin, numbers of CFU mirrored the changes observed in the microcolony assay. There was a statistically significant decrease in H37Ra CFU compared to virulent strains after treatment with streptomycin. These differences between H37Ra and virulent strains in human fibroblasts suggest that H37Ra may be lacking a virulence determinant involved in cell-to-cell spread ofM. tuberculosis.
37
Boldogköi, Zsolt, Ferenc Erdélyi e István Fodor. "A putative latency promoter/enhancer (PLAT2) region of pseudorabies virus contains a virulence determinant". Microbiology 81, n. 2 (1 febbraio 2000): 415–20. http://dx.doi.org/10.1099/0022-1317-81-2-415.
Abstract (sommario):
Contradictory data have recently been reported on the role of the unique long–internal repeat junction area of pseudorabies (Aujeszky’s disease) virus (PrV) genome in the virulence of the virus. To investigate the basis of the difference, four recombinant PrVs mutated at the outer region of inverted repeats that involved a putative latency promoter (PLAT2) were constructed in this study. Propagation characteristics of mutant viruses in cultured cells were similar to those of the wild-type virus. However, a 757 bp deletion at this location caused significant reduction in the virulence of PrV after intraperitoneal inoculation of mice and a moderate decrease in the virulence after intracranial inoculation. These results indicate that the PLAT2 region is an important virulence determinant that may be implicated in the neuroinvasive capability of the virus.
38
MORENO, E., A. ANDREU, T. PÉREZ, M. SABATÉ, J. R. JOHNSON e G. PRATS. "Relationship between Escherichia coli strains causing urinary tract infection in women and the dominant faecal flora of the same hosts". Epidemiology and Infection 134, n. 5 (26 gennaio 2006): 1015–23. http://dx.doi.org/10.1017/s0950268806005917.
Abstract (sommario):
To clarify whether prevalence or special pathogenicity is more important in determining urinary tract infection (UTI) causation, we compared the biotype, phylogenetic group, and virulence genes of Escherichia coli urine strains from 11 women with acute lower UTI with those of the host's dominant intestinal E. coli strain(s). Twenty-one unique E. coli clones were identified. For three women, the single faecal clone identified was also the host's urine clone, whereas for eight women faecal samples yielded 1 or 2 distinct non-urine clones (total, n=10), either with (n=3) or without (n=5) the concurrent urine clone. The eight urine clones from the latter eight women exhibited significantly greater inferred virulence, according to virulence gene content and phylogenetic background, than did the hosts' 10 corresponding ‘faecal only’ clones. In contrast, the three urine clones that were detected as the host's sole faecal clone exhibited significantly lower inferred virulence than the other eight urine clones, and were statistically indistinguishable from the 10 ‘faecal only’ clones. In conclusion, special pathogenicity is an important determinant of UTI pathogenesis in women, although prevalence may occasionally allow less virulent strains to cause UTI.
39
McCarthy, Alex J., Patricia Martin, Emilie Cloup, Richard A. Stabler, Eric Oswald e Peter W. Taylor. "The Genotoxin Colibactin Is a Determinant of Virulence in Escherichia coli K1 Experimental Neonatal Systemic Infection". Infection and Immunity 83, n. 9 (6 luglio 2015): 3704–11. http://dx.doi.org/10.1128/iai.00716-15.
Abstract (sommario):
Escherichia colistrains expressing the K1 capsule are a major cause of sepsis and meningitis in human neonates. The development of these diseases is dependent on the expression of a range of virulence factors, many of which remain uncharacterized. Here, we show that all but 1 of 34E. coliK1 neonatal isolates carriedclbAandclbP, genes contained within thepkspathogenicity island and required for the synthesis of colibactin, a polyketide-peptide genotoxin that causes genomic instability in eukaryotic cells by induction of double-strand breaks in DNA. Inactivation ofclbAandclbPinE. coliA192PP, a virulent strain of serotype O18:K1 that colonizes the gastrointestinal tract and translocates to the blood compartment with very high frequency in experimental infection of the neonatal rat, significantly reduced the capacity of A192PP to colonize the gut, engender double-strand breaks in DNA, and cause invasive, lethal disease. Mutation ofclbA, which encodes a pleiotropic enzyme also involved in siderophore synthesis, impacted virulence to a greater extent than mutation ofclbP, encoding an enzyme specific to colibactin synthesis. Restoration of colibactin gene function by complementation reestablished the fully virulent phenotype. We conclude that colibactin contributes to the capacity ofE. coliK1 to colonize the neonatal gastrointestinal tract and to cause invasive disease in the susceptible neonate.
40
Bailey, D., L. B. Thackray e I. G. Goodfellow. "A Single Amino Acid Substitution in the Murine Norovirus Capsid Protein Is Sufficient for Attenuation In Vivo". Journal of Virology 82, n. 15 (21 maggio 2008): 7725–28. http://dx.doi.org/10.1128/jvi.00237-08.
Abstract (sommario):
ABSTRACT Murine norovirus (MNV), a prevalent pathogen of laboratory mice, shares many characteristics with human noroviruses. Previous results indicated that passage of MNV1 in the macrophage cell line RAW 264.7 results in attenuation in STAT1-deficient mice (C. E. Wobus, S. M. Karst, L. B. Thackray, K. O. Chang, S. V. Sosnovtsev, G. Belliot, A. Krug, J. M. Mackenzie, K. Y. Green, and H. W. Virgin, PLoS. Biol. 2:e432, 2004). Sequence analysis revealed two amino acid differences between the virulent and attenuated viruses. Using an infectious cDNA clone of the attenuated virus, we demonstrated that a glutamate-to-lysine substitution at position 296 in the capsid protein (VP1) is sufficient to restore virulence in vivo, identifying, for the first time, a virus-encoded molecular determinant of norovirus virulence.
41
Reckseidler, Shauna L., David DeShazer, Pamela A. Sokol e Donald E. Woods. "Detection of Bacterial Virulence Genes by Subtractive Hybridization: Identification of Capsular Polysaccharide ofBurkholderia pseudomallei as a Major Virulence Determinant". Infection and Immunity 69, n. 1 (1 gennaio 2001): 34–44. http://dx.doi.org/10.1128/iai.69.1.34-44.2001.
Abstract (sommario):
ABSTRACT Burkholderia pseudomallei, the etiologic agent of melioidosis, is responsible for a broad spectrum of illnesses in humans and animals particularly in Southeast Asia and northern Australia, where it is endemic. Burkholderia thailandensisis a nonpathogenic environmental organism closely related to B. pseudomallei. Subtractive hybridization was carried out between these two species to identify genes encoding virulence determinants in B. pseudomallei. Screening of the subtraction library revealed A-T-rich DNA sequences unique toB. pseudomallei, suggesting they may have been acquired by horizontal transfer. One of the subtraction clones, pDD1015, encoded a protein with homology to a glycosyltransferase fromPseudomonas aeruginosa. This gene was insertionally inactivated in wild-type B. pseudomallei to create SR1015. It was determined by enzyme-linked immunosorbent assay and immunoelectron microscopy that the inactivated gene was involved in the production of a major surface polysaccharide. The 50% lethal dose (LD50) for wild-type B. pseudomallei is <10 CFU; the LD50 for SR1015 was determined to be 3.5 × 105 CFU, similar to that of B. thailandensis (6.8 × 105CFU). DNA sequencing of the region flanking the glycosyltransferase gene revealed open reading frames similar to capsular polysaccharide genes in Haemophilus influenzae,Escherichia coli, and Neisseria meningitidis. In addition, DNA from Burkholderia mallei andBurkholderia stabilis hybridized to a glycosyltransferase fragment probe, and a capsular structure was identified on the surface of B. stabilis via immunoelectron microscopy. Thus, the combination of PCR-based subtractive hybridization, insertional inactivation, and animal virulence studies has facilitated the identification of an important virulence determinant in B. pseudomallei.
42
Nickells, Janice, Maria Cannella, Deborah A. Droll, Yan Liang, William S. M. Wold e Thomas J. Chambers. "Neuroadapted Yellow Fever Virus Strain 17D: a Charged Locus in Domain III of the E Protein Governs Heparin Binding Activity and Neuroinvasiveness in the SCID Mouse Model". Journal of Virology 82, n. 24 (8 ottobre 2008): 12510–19. http://dx.doi.org/10.1128/jvi.00458-08.
Abstract (sommario):
ABSTRACT A molecular clone of yellow fever virus (YFV) strain 17D was used to identify critical determinants of mouse neuroinvasiveness previously localized to domain III of the neuroadapted SPYF-MN virus envelope protein. Three candidate virulence substitutions (305F→V, 326K→E, and 380R→T) were individually evaluated for their roles in this phenotype in a SCID mouse model. The virus containing a glutamic acid residue at position 326 of the envelope protein (326E) caused rapidly lethal encephalitis, with a mortality rate and average survival time resembling those of the parental SPYF-MN virus. Determinants at positions 380 (380T) and 305 (305V) did not independently affect neuroinvasiveness. Testing a panel of viruses with various amino acid substitutions at position 326 revealed that attenuation of neuroinvasiveness required a positively charged residue (lysine or arginine) at this position. Molecular-modeling studies suggest that residues 326 and 380 contribute to charge clusters on the lateral surface of domain III that constitute putative heparin binding sites, as confirmed by studies of heparin inhibition of plaque formation. The neuroinvasiveness of YFVs in the SCID model correlated inversely with sensitivity to heparin. These findings establish that residue 326 in domain III of the E protein is a critical determinant of YFV neuroinvasiveness in the SCID mouse model. Together with modeling of domain III from virulent YFV strains, the data suggest that heparin binding activity involving lysine at position 326 may be a modulator of YFV virulence phenotypes.
43
Lee, Eva, e Mario Lobigs. "E Protein Domain III Determinants of Yellow Fever Virus 17D Vaccine Strain Enhance Binding to Glycosaminoglycans, Impede Virus Spread, and Attenuate Virulence". Journal of Virology 82, n. 12 (9 aprile 2008): 6024–33. http://dx.doi.org/10.1128/jvi.02509-07.
Abstract (sommario):
ABSTRACT The yellow fever virus (YFV) 17D strain is one of the most effective live vaccines for human use, but the in vivo mechanisms for virulence attenuation of the vaccine and the corresponding molecular determinants remain elusive. The vaccine differs phenotypically from wild-type YFV by the loss of viscerotropism, despite replicative fitness in cell culture, and genetically by 20 amino acid changes predominantly located in the envelope (E) protein. We show that three residues in E protein domain III inhibit spread of 17D in extraneural tissues and attenuate virulence in type I/II interferon-deficient mice. One of these residues (Arg380) is a dominant glycosaminoglycan-binding determinant, which mainly accounts for more rapid in vivo clearance of 17D from the bloodstream in comparison to 17D-derived variants with wild-type-like E protein. While other mutations will account for loss of neurotropism and phenotypic stability, the described impact of E protein domain III changes on virus dissemination and virulence is the first rational explanation for the safety of the 17D vaccine in humans.
44
Ozanic, Mateja, Valentina Marecic, Masa Knezevic, Ina Kelava, Pavla Stojková, Lena Lindgren, Jeanette E. Bröms, Anders Sjöstedt, Yousef Abu Kwaik e Marina Santic. "The type IV pili component PilO is a virulence determinant of Francisella novicida". PLOS ONE 17, n. 1 (25 gennaio 2022): e0261938. http://dx.doi.org/10.1371/journal.pone.0261938.
Abstract (sommario):
Francisella tularensis is a highly pathogenic intracellular bacterium that causes the disease tularemia. While its ability to replicate within cells has been studied in much detail, the bacterium also encodes a less characterised type 4 pili (T4P) system. T4Ps are dynamic adhesive organelles identified as major virulence determinants in many human pathogens. In F. tularensis, the T4P is required for adherence to the host cell, as well as for protein secretion. Several components, including pilins, a pili peptidase, a secretin pore and two ATPases, are required to assemble a functional T4P, and these are encoded within distinct clusters on the Francisella chromosome. While some of these components have been functionally characterised, the role of PilO, if any, still is unknown. Here, we examined the role of PilO in the pathogenesis of F. novicida. Our results show that the PilO is essential for pilus assembly on the bacterial surface. In addition, PilO is important for adherence of F. novicida to human monocyte-derived macrophages, secretion of effector proteins and intracellular replication. Importantly, the pilO mutant is attenuated for virulence in BALB/c mice regardless of the route of infection. Following intratracheal and intradermal infection, the mutant caused no histopathology changes, and demonstrated impaired phagosomal escape and replication within lung liver as well as spleen. Thus, PilO is an essential virulence determinant of F. novicida.
45
MARTÍN, MARÍA, JORGE GUTIÉRREZ, RAQUEL CRIADO, CARMEN HERRANZ, LUIS M. CINTAS e PABLO E. HERNÁNDEZ. "Genes Encoding Bacteriocins and Their Expression and Potential Virulence Factors of Enterococci Isolated from Wood Pigeons (Columba palumbus)". Journal of Food Protection 69, n. 3 (1 marzo 2006): 520–31. http://dx.doi.org/10.4315/0362-028x-69.3.520.
Abstract (sommario):
Samples of the intestinal content and carcasses of wood pigeons (Columba palumbus) were evaluated for enterococci with antimicrobial activity. Enterococcus faecium comprised the largest enterococcal species with antagonistic activity, followed by Enterococcus faecalis and Enterococcus columbae. PCR amplification of genes coding bacteriocins and determination of their nucleotide sequence, and the use of specific antipeptide bacteriocin antibodies and a noncompetitive indirect enzyme-linked immunosorbent assay, permitted characterization of enterococci coding that described bacteriocins and their expression. The efaAfm determinant was the only virulence gene detected in E. faecium, whereas E. faecalis showed a larger number of virulence determinants, and E. columbae did not carry any of the virulence genes examined. Although all E. faecalis isolates manifested a potent direct antimicrobial activity, no activity was detected in supernatants of producer cells. Purification of the antagonistic activity of E. columbae PLCH2 showed multiple chromatographic fragments after matrix-assisted laser desorption–ionization time-of-flight mass spectrometry analysis, suggesting the active peptide(s) had not yet purified to homogeneity. Bacteriocinogenic E. faecium and E. columbae isolates may be considered hygienic for production of enterocins and potentially safe due to their low incidence of potential virulence genes and susceptibility of most relevant clinical antibiotics. However, the presence among the enterococci of E. faecalis strains with a potent antagonistic activity and multiple virulence factors is an issue that must be considered further.
46
Ahangaran, Akbar, Mina Koohi Habibi, Gholam-Hossein Mosahebi Mohammadi, Stephan Winter e Fernando García-Arenal. "Analysis of Soybean mosaic virus genetic diversity in Iran allows the characterization of a new mutation resulting in overcoming Rsv4-resistance". Journal of General Virology 94, n. 11 (1 novembre 2013): 2557–68. http://dx.doi.org/10.1099/vir.0.055434-0.
Abstract (sommario):
The genetic variation and population structure of Soybean mosaic virus (SMV) in Iran was analysed through the characterization of a set of isolates collected in the soybean-growing provinces of Iran. The partial nucleotide sequence of these isolates showed a single, undifferentiated population with low genetic diversity, highly differentiated from other SMV world populations. These traits are compatible with a population bottleneck associated with the recent introduction of SMV in Iran. Phylogenetic analyses suggest that SMV was introduced into Iran from East Asia, with at least three introduction events. The limited genetic diversification of SMV in Iran may be explained by strong negative selection in most viral genes eliminating the majority of mutations, together with recombination purging deleterious mutations. The pathogenicity of Iranian SMV isolates was typified on a set of soybean differential lines either susceptible or carrying different resistance genes or alleles to SMV. Two pathotypes were distinguished according to the ability to overcome Rsv4 resistance in line V94-5152. Amino acid sequence comparisons of virulent and avirulent isolates on V94-5152 (Rsv4), plus site-directed mutagenesis in a biologically active cDNA clone, identified mutation S1053N in the P3 protein as the determinant for virulence on V94-5152. Codon 1053 was shown to be under positive selection, and S1053N-determined Rsv4-virulence occurred in isolates with different genealogies. The V94-5152 (Rsv4)-virulence determinant in Iranian isolates maps into a different amino acid position in the P3 protein than those previously reported, indicating different evolutionary pathways towards resistance breaking that might be conditioned by sequence context.
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Boyce, John D., e Ben Adler. "The Capsule Is a Virulence Determinant in the Pathogenesis of Pasteurella multocida M1404 (B:2)". Infection and Immunity 68, n. 6 (1 giugno 2000): 3463–68. http://dx.doi.org/10.1128/iai.68.6.3463-3468.2000.
Abstract (sommario):
ABSTRACT Capsules from a range of pathogenic bacteria are key virulence determinants, and the capsule has been implicated in virulence inPasteurella multocida. We have previously identified and determined the nucleotide sequence of the P. multocidaM1404 (B:2) capsule biosynthetic locus (J. D. Boyce, J. Y. Chung, and B. Adler, Vet. Microbiol. 72:121–134, 2000). Thecap locus consists of 15 genes, which can be grouped into three functional regions. Regions 1 and 3 contain genes proposed to encode proteins involved in capsule export, and region 2 contains genes proposed to encode proteins involved in polysaccharide biosynthesis. In order to construct a mutant impaired in capsule export, the final gene of region 1, cexA, was disrupted by insertion of a tetracycline resistance cassette by allelic replacement. The genotype of the tet(M) ΩcexA mutant was confirmed by Southern hybridization and PCR. The acapsular phenotype was confirmed by immunofluorescence, and the strain could be complemented and returned to capsule production by the presence of a cloned uninterrupted copy of cexA. Wild-type, mutant, and complemented strains were tested for virulence by intraperitoneal challenge of mice; the presence of the capsule was shown to be a crucial virulence determinant. Following intraperitoneal challenge of mice, the acapsular bacteria were removed efficiently from the blood, spleen, and liver, while wild-type bacteria multiplied rapidly. Acapsular bacteria were readily taken up by murine peritoneal macrophages, but wild-type bacteria were significantly resistant to phagocytosis. Both wild-type and acapsular bacteria were resistant to complement in bovine and murine serum.
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Dhandayuthapani, S., M. W. Blaylock, C. M. Bebear, W. G. Rasmussen e J. B. Baseman. "Peptide Methionine Sulfoxide Reductase (MsrA) Is a Virulence Determinant in Mycoplasma genitalium". Journal of Bacteriology 183, n. 19 (1 ottobre 2001): 5645–50. http://dx.doi.org/10.1128/jb.183.19.5645-5650.2001.
Abstract (sommario):
ABSTRACT Mycoplasma genitalium is the smallest self-replicating microorganism and is implicated in human diseases, including urogenital and respiratory infections and arthritides. M. genitalium colonizes host cells primarily through adherence mechanisms mediated by a network of surface-associated membrane proteins, including adhesins and cytadherence-related proteins. In this paper, we show that cytadherence in M. genitalium is affected by an unrelated protein known as peptide methionine sulfoxide reductase (MsrA), an antioxidant repair enzyme that catalyzes the reduction of methionine sulfoxide [Met(O)] residues in proteins to methionine. An msrA disruption mutant of M. genitalium, constructed through homologous recombination, displayed markedly reduced adherence to sheep erythrocytes. In addition, the msrA mutant was incapable of growing in hamsters and exhibited hypersensitivity to hydrogen peroxide when compared to wild-type virulent M. genitalium. These results indicate that MsrA plays an important role in M. genitalium pathogenicity, possibly by protecting mycoplasma protein structures from oxidative damage or through alternate virulence-related pathways.
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Simmons, Jason D., Amy C. Wollish e Mark T. Heise. "A Determinant of Sindbis Virus Neurovirulence Enables Efficient Disruption of Jak/STAT Signaling". Journal of Virology 84, n. 21 (25 agosto 2010): 11429–39. http://dx.doi.org/10.1128/jvi.00577-10.
Abstract (sommario):
ABSTRACT Previous studies with Venezuelan equine encephalitis virus and Sindbis virus (SINV) indicate that alphaviruses are capable of suppressing the cellular response to type I and type II interferons (IFNs) by disrupting Jak/STAT signaling; however, the relevance of this signaling inhibition toward pathogenesis has not been investigated. The relative abilities of neurovirulent and nonneurovirulent SINV strains to downregulate Jak/STAT signaling were compared to determine whether the ability to inhibit IFN signaling correlates with virulence potential. The adult mouse neurovirulent strain AR86 was found to rapidly and robustly inhibit tyrosine phosphorylation of STAT1 and STAT2 in response to IFN-γ and/or IFN-β. In contrast, the closely related SINV strains Girdwood and TR339, which do not cause detectable disease in adult mice, were relatively inefficient inhibitors of STAT1/2 activation. Decreased STAT activation in AR86-infected cells was associated with decreased activation of the IFN receptor-associated tyrosine kinases Tyk2, Jak1, and Jak2. To identify the viral factor(s) involved, we infected cells with several panels of AR86/Girdwood chimeric viruses. Surprisingly, we found that a single amino acid determinant, threonine at nsP1 position 538, which is required for AR86 virulence, was also required for efficient disruption of STAT1 activation, and this determinant fully restored STAT1 inhibition when it was introduced into the avirulent Girdwood background. These data indicate that a key virulence determinant plays a critical role in downregulating the response to type I and type II IFNs, which suggests that the ability of alphaviruses to inhibit Jak/STAT signaling relates to their in vivo virulence potential.
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Risatti, G. R., M. V. Borca, G. F. Kutish, Z. Lu, L. G. Holinka, R. A. French, E. R. Tulman e D. L. Rock. "The E2 Glycoprotein of Classical Swine Fever Virus Is a Virulence Determinant in Swine". Journal of Virology 79, n. 6 (15 marzo 2005): 3787–96. http://dx.doi.org/10.1128/jvi.79.6.3787-3796.2005.
Abstract (sommario):
ABSTRACT To identify genetic determinants of classical swine fever virus (CSFV) virulence and host range, chimeras of the highly pathogenic Brescia strain and the attenuated vaccine strain CS were constructed and evaluated for viral virulence in swine. Upon initial screening, only chimeras 138.8v and 337.14v, the only chimeras containing the E2 glycoprotein of CS, were attenuated in swine despite exhibiting unaltered growth characteristics in primary porcine macrophage cell cultures. Additional viral chimeras were constructed to confirm the role of E2 in virulence. Chimeric virus 319.1v, which contained only the CS E2 glycoprotein in the Brescia background, was markedly attenuated in pigs, exhibiting significantly decreased virus replication in tonsils, a transient viremia, limited generalization of infection, and decreased virus shedding. Chimeras encoding all Brescia structural proteins in a CS genetic background remained attenuated, indicating that additional mutations outside the structural region are important for CS vaccine virus attenuation. These results demonstrate that CS E2 alone is sufficient for attenuating Brescia, indicating a significant role for the CSFV E2 glycoprotein in swine virulence.