Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “virulence evolution”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed1999

The SPI-3 pathogenicity island of Salmonella enterica.

Pathogenicity islands are chromosomal clusters of pathogen-specific virulence genes often found at tRNA loci. We have determined the molecular genetic structure of SPI-3, a 17-kb pathogenicity island located at the selC tRNA locus of Salmonella enterica serovar Typhimurium. The G+C content of SPI-3 (47.5%) differs from that of the Salmonella genome (52%), consistent with the notion that these sequences have been horizontally acquired. SPI-3 harbors 10 open reading frames organized in six transcriptional units, which include the previously described mgtCB operon encoding the macrophage survival protein MgtC and the Mg2+ transporter MgtB. Among the newly identified open reading frames, one exhibits sequence similarity to the ToxR regulatory protein of Vibrio cholerae and one is similar to the AIDA-I adhesin of enteropathogenic Escherichia coli. The distribution of SPI-3 sequences varies among the salmonellae: the right end of the island, which harbors the virulence gene mgtC, is present in all eight subspecies of Salmonella; however, a four-gene cluster at the center of SPI-3 is found in only some of the subspecies and is bracketed by remnants of insertion sequences, suggesting a multistep process in the evolution of SPI-3 sequences.

Adenosine Triphosphatases↗
PubMedDate not supplied

[The population genetics of nodule bacteria].

The data are reviewed on the population structure and evolutionary dynamics of the nodule bacteria (rhizobia) which are among the most intensively studied microorganisms. High level of the population polymorphism was demonstrated for the rhizobia populations using the enzyme electrophoresis (MLEE profiles). The average value of Nei's coefficient of heterogeneity (H = 1 - sigma pi2 [n/(n - 1)]) were: 0.590 for rhizobia (Rhizobium, Bradyrhizobium), 0.368 for enterobacteria (Escherichia, Salmonella, Shigella) and 0.452 for pathogenic bacteria (Bordetella, Borrelia, Erysipelothrix, Haemophilus, Helicobacter, Listeria, Mycobacterium, Neisseria, Staphylococcus) populations. In spite of being devoid of the effective systems for the gene conjugative transfer, many rhizobia populations possess an essentially panmictic structure. However, the enterobacteria populations in which the gene transfer may be facilitated due to the conjugative F- and R-factors, usually display the clonal population structure. The legume host plant is proved to be a key factor that determines the high levels of polymorphism and of panmixis as well as high evolutionary rates of the symbiotic bacteria populations. The host may ensure: a) an increase in mutation and gene transfer frequencies; b) stimulation of the competitive (selective) processes in both symbiotic and free-living rhizobia populations. A "cyclic" model of the rhizobia microevolution is presented which allows to assess the inputs the interstrain competition for the saprophytic growth and for the host nodulation into evolution of a plant-associated rhizobia population. The nodulation competitiveness in the rhizobia populations is responsible for the frequency-dependent selection of the rare genotypes which may arise in the soil bacterial communities as a result of the transfer of symbiotic (sym) genes from virulent rhizobia strains to either avirulent rhizobia or to the other (saprophytic, phytopathogenic) bacteria. Therefore, the nodulation competitiveness may ensure: a) panmictic structure of the natural rhizobia populations; b) high taxonomic diversity of rhizobia which was apparently caused by a broad sym gene expansion in the soil bacterial communities. The kin selection models are presented which explain evolution of the "altruistic" (essential for the host plant, but not for the bacteria themselves) symbiotic traits (e.g., the ability for symbiotic nitrogen fixation and for differentiation into non-viable bacteroids) in the rhizobia populations. These models are based on preferential multiplication of the nitrogen-fixing clones either in planta (due to an elevated supply of the nitrogen-fixing nodules with photosynthates) or ex planta (due to a release of the rhizopines from the nitrogen-fixing nodules). Speaking generally, interactions with the host plants provide a range of mechanisms increasing a genetic heterogeneity and an evolutionary potential in the associated rhizobia populations.

Altruism↗
PubMed2002

Detection of recombination among Salmonella enterica strains using the incongruence length difference test.

Particular serovars of Salmonella enterica have emerged as significant foodborne pathogens in humans. At the chromosomal level, discrete regions in the Salmonella genome have been identified that are known to play important roles in the maintenance, survival, and virulence of S. enterica within the host. Interestingly, several of these loci appear to have been acquired by horizontal transfer of DNA among and between bacterial species. The profound importance of recombination in pathogen emergence is just now being realized, perhaps explaining the sudden interest in developing novel and facile ways for detecting putative horizontal transfer events in bacteria. The incongruence length difference (ILD) test offers one such means. ILD uses phylogeny to trace sequences that may have been acquired promiscuously by exchange of DNA during chromosome evolution. We show here that the ILD test readily detects recombinations that have taken place in several housekeeping genes in Salmonella as well as genes composing the type 1 pilin complex (14 min) and the inv-spa invasion gene complex (63 min). Moreover, the ILD test indicated that the mutS gene (64 min), whose product helps protect the bacterial genome from invasion by foreign DNA, appears to have undergone intragenic recombination within S. enterica subspecies I. ILD findings were supported using additional tests known to be independent of the ILD approach (e.g., split decomposition analysis and compatibility of sites). Taken together, these data affirm the application of the ILD test as one approach for identifying recombined sequences in the Salmonella chromosome. Furthermore, horizontally acquired sequences within mutS support a model whereby evolutionarily important recombinants of S. enterica are rescued from strains carrying defective mutS alleles via horizontal transfer.

Adenosine Triphosphatases↗
PubMed2002

Pathogenic fungal species hybrids infecting plants.

In this review, we give a summary of recent examples of hybridisation in fungi. Reports on hybridisation between pathogenic fungi infecting plants have increased during the last decade. Hybrids of plant pathogens may create devastating new diseases on both cultivated and wild plants; at the same time, hybridisation is one of the natural processes in the course of evolution of new taxa.

Fungi↗
PubMed1998

Genome sequence of an obligate intracellular pathogen of humans: Chlamydia trachomatis.

Analysis of the 1,042,519-base pair Chlamydia trachomatis genome revealed unexpected features related to the complex biology of chlamydiae. Although chlamydiae lack many biosynthetic capabilities, they retain functions for performing key steps and interconversions of metabolites obtained from their mammalian host cells. Numerous potential virulence-associated proteins also were characterized. Several eukaryotic chromatin-associated domain proteins were identified, suggesting a eukaryotic-like mechanism for chlamydial nucleoid condensation and decondensation. The phylogenetic mosaic of chlamydial genes, including a large number of genes with phylogenetic origins from eukaryotes, implies a complex evolution for adaptation to obligate intracellular parasitism.

Aerobiosis↗
PubMed1996

High mutation frequencies among Escherichia coli and Salmonella pathogens.

Here it is reported that the incidence of mutators among isolates of pathogenic Escherichia coli and Salmonella enterica is high (over 1 percent). These findings counter the theory, founded on studies with laboratory-attenuated strains, that suggests mutators are rare among bacterial populations. Defects in methyl-directed mismatch repair underlie all mutator phenotypes described here. Of nine independently derived hypermutable strains, seven contained a defective mutS allele. Because these mutant alleles increase the mutation rate and enhance recombination among diverse species, these studies may help explain both the rapid emergence of antibiotic resistance and the penetrance of virulence genes within the prokaryotic community.

Adenosine Triphosphatases↗
PubMed2004

In vitro recombinants of two nearly identical potyviral isolates express novel virulence and symptom phenotypes in plants.

Six novel chimeric viruses were constructed by sequentially exchanging segments of the viral genomes between the infectious cDNA clone (pPVA-B11) of Potato virus A (isolate PVA-B11) and pUFL, an almost identical infectious cDNA of PVA (isolate U) made in this study. The infectious in vitro transcripts of pUFL and pPVA-B11 caused similar severe mosaic and leaf malformation phenotypes in systemically infected leaves of Nicotiana benthamiana. In contrast, one chimera induced a unique phenotype of yellow vein chlorosis without leaf malformation with viral titres that were equivalent to those of the parental viruses. Furthermore, as opposed to the viral cDNAs from which it was assembled, one chimera showed no detectable infectivity of N. benthamiana plants. Thus, recombination of nearly identical, phenotypically similar virus genomes can give rise to new viral strains with novel virulence and symptom phenotypes, which has not previously been demonstrated with potyviruses. One chimera failed to cause systemic infection in potato plants, but, nevertheless, avirulence could not be attributed to a single genomic region. These data suggest that different parts of the potyviral genome function coordinately. The results provide novel insights into the evolution of the genus Potyvirus.

Cloning, Molecular↗
PubMed2006

A preliminary panorama of the diversity of N1 subtype influenza viruses.

N1 subtype influenza viruses have caused many epidemics and even a few pandemics in humans, pigs and fowls including 1918 human H1N1 pandemic, which killed 20-50 million people and the current avian H5N1 pandemic in the Eastern Hemisphere, which has caused great economic losses and posed a severe threat to human public health. To elucidate the whole diversity of N1 influenza viruses from a dynamic view, 202 neuraminidase (NA) sequences of N1 subtype influenza isolates were selected and analyzed in this study. Our results showed that N1 influenza isolates could be divided into three distinct lineages (Human, Classic Swine and Avian), which largely circulated in the humans, pigs and fowls respectively, though viruses in the Avian lineage could infect mammals and even there was a sublineage in the Avian lineage wholly isolated from pigs. The Avian lineage and the Human lineage, which have existed at least for decades, possibly began divergence around in 1890 through regression analysis. Both of the Human and Avian lineages could be further divided into some sublineages, and the correlation between these lineages (or sublineages) and their isolation places, isolation time, hemagglutinin (HA) subtypes, host species, virulence, or epidemics were discussed. The panorama of the diversity of N1 influenza viruses presented in this study provided a framework for the studies on the evolution and epidemiology of N1 influenza viruses.

Amino Acid Sequence↗
PubMed2004

A framework for understanding the potential for emerging diseases in aquaculture.

Numerous diseases have emerged as serious economic or ecological problems in aquaculture species. The combination of factors behind the emergence of each disease is unique, but various common factors are apparent. We combine risk-analysis methods and virulence theory with historical examples (mainly from salmonid production) to identify key disease-emergence risk factors. Diseases have emerged through pathogen exchange with wild populations, evolution from non-pathogenic micro-organisms and anthropogenic transfer of stocks. Aquacultural practices frequently result in high population densities and other stresses (such as intercurrent disease) which increase the risk of infection establishment and spread. As aquaculture expands and new species are farmed, diseases will continue to emerge and affect both wild and farmed fish adversely. The rate and extent of emergence can be reduced by the application of biosecurity programmes designed to mitigate the risk factors for disease emergence.

Animals↗
PubMed2003

Limited evolution of West Nile virus has occurred during its southwesterly spread in the United States.

Analysis of partial nucleotide sequences of nine West Nile virus strains isolated in southeast Texas during June-August 2002 revealed a maximum of 0.35% nucleotide variation from a New York 1999 strain. Two sequence subtypes were identified that differed from each other by approximately 0.5%, suggesting multiple introductions of virus to this area. Analysis of sequences from cloned PCR products for one strain revealed up to 0.6% divergence from the consensus sequence at the subpopulation level. The presence of unique patterns of small numbers of mutations in North American West Nile strains studied to date may suggest the absence of a strong selective pressure to drive the emergence of dominant variants.

Animals↗
PubMedDate not supplied

Emergence of Salmonella epidemics: the problems related to Salmonella enterica serotype Enteritidis and multiple antibiotic resistance in other major serotypes.

Two major changes in the epidemiology of salmonellosis occurred in the second half of the 20th century: the emergence of food-borne human infections caused by S. Enteritidis and by multiple-antibiotic resistant strains of Salmonella. This review updates information on the S. Enteritidis pandemic and focuses on the emergence of Salmonella, carrying the SGI1 antibiotic resistance gene cluster, resistant to extended-spectrum cephalosporins, or resistant to fluoroquinolones. The factors responsible for the emergence of these Salmonella strains could be either of human origin or related to bacterial genome evolution. However, our increasing understanding of the molecular fluidity of the genome shows that any attempt to counteract bacteria results in further bacterial evolution or adaptation of other bacteria to take place in the new free ecological niche. In these conditions, we can ask who is faster: humans who want to eliminate bacterial pathogens or bacteria that continuously evolve to gain new niches.

Animals↗
PubMed2000

Evolving superantigens of Staphylococcus aureus.

Staphylococcus aureus bacteria utilize an extensive array of molecular countermeasures to manipulate the defensive microenvironment of the infected host and colonize potentially any tissue. The secreted polypeptides referred to as superantigens are unique among these countermeasures, because they target the multireceptor communication between T cells and antigen-presenting cells that is fundamental to initiating pathogen-specific immune clearance. Superantigens play a critical role in toxic-shock syndrome and food poisoning, yet their function in routine infections is not well understood. While an association of superantigens with cases of human autoimmune disease seems tantalizing, convincing data are not yet available. Blocking antigen-specific T-cell recognition is the primary evolutionary driving force behind superantigen selection, whereas superantigen-specific pathologies are by-products that are apparent only under select conditions.

Antigen-Presenting Cells↗
PubMed2001

The ecology of genetically diverse infections.

Microparasite infections often consist of genetically distinct clonal lineages. Ecological interactions between these lineages within hosts can influence disease severity, epidemiology, and evolution. Many medical and veterinary interventions have an impact on genetic diversity within infections, but there is little understanding of the long-term consequences of such interventions for public and animal health. Indeed, much of the theory in this area is based on assumptions contradicted by the available data.

Animals↗
PubMed2000

Parasitology. Close encounters: good, bad, and ugly.

Microbiologists often focus on one organism and its relationship to its host at one point in time. But viewed in light of evolution, host-parasite relationships range from deadly to helpful, depending on the communication between them. At a meeting here last month of virologists, bacteriologists, parasitologists, and molecular biologists--each dealing with different microorganisms in distinct ways--researchers lamented that evolution is often considered outside the bailiwick of microbiologists, particularly those studying infectious diseases.

Animals↗
PubMed2005

The IncP island in the genome of Brucella suis 1330 was acquired by site-specific integration.

An 18,228-bp region containing open reading frames predicted to be derived from the IncP plasmid or phage ancestors is present in the genomes of Brucella suis biovars 1 to 4, B. canis, B. neotomae, and strains isolated from marine mammals, but not in B. melitensis, B. abortus, B. ovis, and B. suis biovar 5. The presence of circular excision intermediates and the results of an analysis of sequenced bacterial genomes suggest that the region downstream of the guaA gene is a hotspot for site-specific integration of foreign DNA mediated by a CP4-like integrase.

Base Sequence↗
PubMed1999

Contributions of genome sequencing to understanding the biology of Helicobacter pylori.

About half of the world's population carries Helicobacter pylori, a gram-negative, spiral bacterium that colonizes the human stomach. The link between H. pylori and, ulceration as well as its association with the development of both gastric cancer and mucosa-associated lymphoid tissue lymphoma in humans is a serious public health concern. The publication of the genome sequences of two stains of H. pylori gives rise to direct evidence on the genetic diversity reported previously with respect to gene organization and nucleotide variability from strain to strain. The genome size of H. pylori strain 26695 is 1,6697,867 bp and is 1,643,831 bp for strain J99. Approximately 89% of the predicted open reading frames are common to both of the strains, confirming H. pylori as a single species. A region containing approximately 45% of H. pylori strain-specific open reading frames, termed the plasticity zone, is present on the chromosomes, verifying that some strain variability exists. Frequent alteration of nucleotides in the third position of the triplet codons and various copies of insertion elements on the individual chromosomes appear to contribute to distinct polymorphic fingerprints among strains analyzed by restriction fragment length polymorphisms, random amplified polymorphic DNA method, and repetitive element-polymerase chain reaction. Disordered chromosomal locations of some genes seen by pulsed-field gel electrophoresis are likely caused by rearrangement or inversion of certain segments in the genomes. Cloning and functional characterization of the genes involved in acidic survival, vacuolating toxin, cag-pathogenicity island, motility, attachment to epithelial cells, natural transformation, and the biosynthesis of lipopolysaccharides have considerably increased our understanding of the molecular genetic basis for the pathogenesis of H. pylori. The homopolymeric nucleotide tracts and dinucleotide repeats, which potentially regulate the on- and off-status of the target genes by the strand-slipped mispairing mechanism, are often found in the genes encoding the outer-membrane proteins, in enzymes for lipopolysaccharide synthesis, and within DNA modification/restriction systems. Therefore, these genes may be involved in the H. pylori-host interaction.

Amino Acid Sequence↗