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 793 records · Page 44Linked to original sources

Coevolution of host and pathogen populations in the Hordeum vulgare-Rhynchosporium secalis pathosystem.

Isolates of Rhynchosporium secalis collected from two experimental barley populations were scored for putative isozyme, colony color, and virulence loci. Allelic frequencies, multilocus haplotype frequencies, and multilocus genetic structure differed in the two populations of R. secalis; haplotypes also differed widely from each other in virulence. The average virulence of isolates collected from the more resistant host population was greater than the average virulence of the isolates collected from the less resistant host population; also the least virulent haplotype, which made up 19% of the pathogen population collected from the less resistant host population, accounted for only 0.3% of the isolates collected from the more resistant host population. It was concluded that the genetic systems of the barley host and fungal pathogen interacted in a complementary fashion and that the genetic structures of both the host and pathogen populations were shaped by coevolutionary processes featuring interactions among loci affecting many different traits, including interactions among host resistance genes and pathogen virulence genes.

Biological Evolution↗

Pathogenicity mechanisms of prokaryotic cells: an evolutionary view.

The success of pathogenic microbes depends on their ability to colonize host tissues and to counter host defense mechanisms. Microorganisms can produce overwhelming infection because of their relatively short generation times, and because they have evolved powerful mechanisms for generating phenotypic diversity as an efficient strategy for adapting to rapidly responding immune system defenses and the broad range of polymorphisms characteristic of different host tissues. Bacterial evolution may not be a continuous process, but more of a succession of temporally spaced major events. These events cause a non-gradual sequence of adaptations to a given environment. The pathogenicity islands are genetically unstable elements, and many of the genes coding for the adhesins, toxins and other virulence factors are present in pathogenicity islands, which almost certainly had former lives as accessory elements or as parts thereof, or were borne on functional accessory elements. Novel genes are also acquired by transduction (mediated by bacteriophages, plasmids or transposons), by conjugation (DNA transfer between cells) or by transformation (natural DNA uptake). Horizontal gene transfer from other species is a major source of variation and is fundamental to the genetic theory of adaptive evolution in prokaryotes.

Bacteria↗

[Study of gametocytes from the Plasmodium "vivax" group: morphology, development in Anopheles and infectivity of Plasmodium yoelii microgametocytes].

The study of the gametocytes of Plasmodium yoelii enabled the differentiation of 4 morphological types: O, I, II and III (in a chronological order) and amongst each of these types the differentiation of healthy and altered gametocytes. These morphological data represent a tool for investigations on the biology of the gametocytes of the "vivax" group. Preliminary experiments bring informations on the evolution of gametocytes and the mechanisms of their infectivity. 1--In experimentaly infected white mice gametocytes of P.y. nigeriensis are infective up to the 3rd-4th day, those of P. y. yoelii until the 5th-6th days. These periods can be shorter when the infection is very virulent or longer when chronical. 2--The drop in infectivity coincides with the increase in number of the altered gametocytes. 3--The loss of infectivity is connected with the condition of the blood: when parasitaemiae are high, it becomes rapidly unsuitable to a normal evolution of the gametocytes: thus, non infective gametocytes acquire a good infectivity in less than two hours when transfered to a clean mouse. 4--The gametocytic composition of the blood taken up by the Anopheles in the capillaries can be very different from that taken at the tail of a Rodent. In the young parasitaemiae, when the Rodents are most infective to the Mosquitoes, there is a considerable enrichment in gametocytes O-I of the blood ingested by the Anopheles as compared to that taken from the Rodents by the usual techniques. This phenomenon could perhaps be explained by the larger size of gametocytes O and I and their retention in the capillaries of the host. 5--The strong infectivity of gametocytes O and I is confirmed by the fact that no infection develops in the Mosquitoes when no such gametocytes are present in the ingested blood. 6--The ageeing of gametocytes appears to be very rapid for gametocytes arising from exo-erythrocytic schizontes reach stage II, 29 hours and stage III, 35 hours, after the rupture of the very first schizonts.

Animals↗

Filamentous phages linked to virulence of Vibrio cholerae.

The pathogenicity of Vibrio cholerae depends upon its production of two key virulence factors: the toxin co-regulated pilus (TCP), a colonization factor, and cholera toxin, an exotoxin. Genes encoding both virulence factors were introduced into V. cholerae by horizontal gene transfer. The toxin genes are contained within the genome of CTXphi, an integrated filamentous phage identified in 1996. In the past few years, it has been shown that CTXphi relies on novel processes for phage DNA integration, replication and secretion. In addition, expression of CTXphi genes--including the toxin genes--and transmission of CTXphi were recently found to be promoted by the antirepressor RstC, which is encoded within RS1, a newly described satellite phage of CTXphi. The genetic island that encodes TCP has also been described as a filamentous phage; however, these sequences are unlike the genome of any previously characterized filamentous phage.

Cholera↗

Cryptococcus neoformans virulence is enhanced after growth in the genetically malleable host Dictyostelium discoideum.

Cryptococcus neoformans is an encapsulated, environmental fungus that can cause life-threatening meningitis. Pathogenicity of C. neoformans for macrophages and vertebrate hosts may be a mechanism selected in evolution for protection against environmental predators. In this study, we investigated whether Dictyostelium discoideum could serve as an alternate host for C. neoformans. D. discoideum has a defined genetic system which provides significant advantages for the study of fungus-amoeba interactions. Our results show that D. discoideum is susceptible to infection with C. neoformans and that the interactions are similar to those described previously for this fungus with macrophages and Acanthamoeba castellanii. Acapsular C. neoformans cells did not replicate when coincubated with D. discoideum. However, incubation of acapsular C. neoformans with D. discoideum mutants defective in myosin VII synthesis resulted in infection, validating the concept that avirulent organisms can be virulent in impaired hosts even at the unicellular level. Phagocytosis of C. neoformans by D. discoideum could be inhibited with capsule-specific antibodies and various sugars. Passage of an encapsulated C. neoformans strain through D. discoideum cultures increased virulence and was accompanied by larger capsules and faster time to melanization. These results add to the evidence implicating soil ameboid predators as important factors for the maintenance of C. neoformans virulence in the environment and suggest that D. discoideum promises to be an extremely useful system for studying the interaction of C. neoformans with phagocytic cells.

Animals↗

Molecular evolution of the F glycoprotein of human parainfluenza virus type 1.

Human parainfluenza virus type 1 (hPIV1) is a major cause of upper and lower respiratory tract infections among children. Immunity is mediated at least in part by antibody to the fusion (F) surface glycoprotein. Thus, genetic variation in the F gene could influence host range, virulence, and immunity. To examine the genetic diversity among hPIV1 isolates, the F genes of hPIV1 isolates from a single geographic location were sequenced and compared with the F gene of a strain isolated in 1957. Genetic variation was 2.2%-3.4%, averaging 0.8 amino acid changes per year. Changes were progressive over time, and virus evolution was dominated by a single lineage. Three of 7 isolates tested did not induce syncytium formation in tissue culture. This phenotype could not be ascribed to a single unique mutation in the F gene, but these 3 isolates had mutations in the transmembrane region of the HN gene. It is unlikely that the limited genetic evolution of the F gene will be an obstacle to vaccine development.

Amino Acid Sequence↗

The panorama of the diversity of H5 subtype influenza viruses.

To elucidate the global diversity of H5 influenza viruses from a dynamic view, haemagglutinin (HA) sequences of 170 isolates were selected and analyzed in this study. Our results showed that H5 influenza isolates could be divided into two distinct lineages that circulated in the Eastern Hemisphere and the Western Hemisphere, respectively. This may be due to the separate migration routes and habitats of birds in the two hemispheres. The two distinct lineages, having existed at least for decades, possibly began divergence in 1850s. Each of the two distinct HA lineages could be further divided into some sublineages, but there was little correlation between the minor lineages and their isolation places, isolation time, neuraminidase subtypes, host species or virulence. The panorama of the diversity of H5 influenza viruses presented here integrated all known H5 epidemics including the current severe H5N1 avian epidemics in the Eastern Hemisphere and suggested that H5 virulent viruses could originate from multiple sublineages and associate with multiple NA subtypes. Our study provided a framework for the studies on the evolution and epidemiology of H5 influenza viruses.

Genetic Variation↗

Phylogenomic and Clinical Perspectives of an East Asia-Specific Cluster of Mycobacterium massiliense.

BACKGROUND: Mycobacterium abscessus subspecies massiliense (MAM) can form genetically related clusters through continuous within-host adaptations. RESEARCH QUESTION: What is the epidemiologic and clinical significance of the sequence type 120 (ST120) strain of MAM, an East Asia-specific cluster? STUDY DESIGN AND METHODS: Isolates were obtained from patients with MAM pulmonary disease at Seoul National University Hospital between October 1, 2019, and December 31, 2023. These isolates were analyzed using multilocus sequence typing and colony morphotyping and were evaluated for glycopeptidolipid biosynthesis-related gene deletions. Whole-genome sequencing was performed for phylogenomic and pangenome analyses, incorporating MAM genome data from public databases. Finally, the clinical course and treatment outcomes of patients infected with ST120 were evaluated. RESULTS: Among the isolates obtained from 136 patients, 50 isolates (36.8%) were classified as ST120. All ST120 isolates exhibited a rough colony morphotype and harbored deletions in glycopeptidolipid biosynthesis-related genes. From 796 global strains, ST120 was identified exclusively in the isolates obtained from South Korea (51/137 isolates [37.1%]), Japan (3/53 [5.7%]), and Taiwan (2/52 [3.8%]). Genomic analysis revealed the stepwise genetic evolution of ST120, suggesting transmission from Taiwan to Japan and from Japan to South Korea. The ST120 strains exhibited genetic mutations associated with virulence and structural alterations within the ESX system. Consequently, patients with ST120 strain infections had a higher prevalence of cavitary disease (23/50 [46%]) than those infected with non-ST120 strains (19/86 [22.1%]; P = .004). Among those who initiated treatment, the proportion of microbiological cure was lower in patients with ST120 infection (6/15 [40.0%]) than in those with non-ST120 infection (24/34 [70.6%]; P = .043). INTERPRETATION: Our results show that ST120, a strain predominantly found in South Korea, is characterized by the extensive loss of glycopeptidolipid biosynthesis-related genes and is associated with increased disease severity and worse treatment outcomes.

Humans↗

Temporal patterns of genetic variation for resistance and infectivity in a Daphnia-microparasite system.

Theoretical studies have indicated that the population genetics of host-parasite interactions may be highly dynamic. with parasites perpetually adapting to common host genotypes and hosts evolving resistance to common parasite genotypes. The present study examined temporal variation in resistance of hosts and infectivity of parasites within three populations of Daphnia magna infected with the sterilizing bacterium Pasteuria ramosa. Parasite isolates and host clones were collected in each of two years (1997, 1998) from one population; in two other populations, hosts were collected from both years, but parasites from only the first year. We then performed infection experiments (separately for each population) that exposed hosts to parasites from the same year or made combinations involving hosts and parasites from different years. In two populations, patterns were consistent with the evolution of host resistance: either infectivity or the speed with which parasites sterilized hosts declined from 1997 to 1998. In another population, infectivity, virulence, and parasite spore production did not vary among host-year or parasite-year. For this population, we also detected strong within-population genetic variation for resistance. Thus, in this case, genetic variability for fitness-related traits apparently did not translate into evolutionary change. We discuss a number of reasons why genetic change may not occur as expected in parasite-host systems, including negative correlations between resistance and other traits, gene flow, or that the dynamic process itself may obscure the detection of gene frequency changes.

Animals↗

Population structure of Enterococcus faecium causing bacteremia in a Spanish university hospital: setting the scene for a future increase in vancomycin resistance?

Over an 8-year period (1995 to 2002), 86 Enterococcus faecium blood isolates from 84 patients, of which 54 were ampicillin resistant (AREF) and 32 were ampicillin susceptible (ASEF), were studied in a university hospital (1,200 beds; serving a population of 600,000) in Spain, a country characterized by a near-absence of resistance to vancomycin and very high rates of ampicillin resistance among enterococci. Clonal relatedness by pulsed-field gel electrophoresis (PFGE), antibiotic susceptibility, presence of the virulence/epidemicity genes esp(Efm) and hyl(Efm), and identification of purK alleles were studied. A group of isolates was also analyzed by amplified fragment length polymorphism (AFLP) and multilocus sequence typing. Medical charts (30 variables collected) were reviewed for 60/84 patients. ASEF showed high clonal diversity (32 PFGE types, 11 purK alleles, 4 AFLP genogroups), did not harbor putative virulence genes, and had no specific association with hospital acquisition. AREF isolates belonged to a clonal complex (CC) of genetically related strains (purK-1, AFLP genogroup C), occasionally harboring putative virulence traits, and were from patients with particular risk factors. Within this CC, previously associated with vancomycin-resistant E. faecium isolates causing outbreaks worldwide (W. L. Homan et al., J. Clin. Microbiol. 40:1963-1971, 2002), a great genetic diversity of antibiotic resistance and virulence/epidemicity profiles was found. Associations between esp and a >7-day hospital stay and between purK-1, hospital location, and nosocomial acquisition were noted (P < 0.001). These findings reflect the importance of local environmental differences in the evolution of this CC, suggesting that the emergence of vancomycin resistance among AREF strains in Spain may be a question of time.

Ampicillin↗

Molecular characterization of a serotype O121:H19 clone, a distinct Shiga toxin-producing clone of pathogenic Escherichia coli.

Most illnesses caused by Shiga toxin-producing Escherichia coli (STEC) have been attributed to E. coli serotype O157:H7, but non-O157 STEC infections are now increasingly recognized as public health problems worldwide. The O121:H19 serotype is being isolated more frequently from clinical specimens and has been implicated in one waterborne outbreak. We used multilocus virulence gene profiling, a PCR-based assay, to characterize the virulence gene content of 24 isolates of serotype O121:H19 and nonmotile variants. We also performed multilocus enzyme electrophoresis and multilocus sequencing to establish the clonal relatedness of O121 isolates and to elucidate the relationship of O121 to common STEC clones. The 24 isolates were found to represent a single bacterial clone, as there was no allelic variation across 18 enzyme loci among the isolates. The complete nucleotide sequence of the intimin gene differed by four substitutions from that of the epsilon (Int- epsilon ) allele of O103:H2 strain PMK5. The typical O121 virulence gene profile was similar to the profiles of enterohemorrhagic E. coli (EHEC) clones of E. coli: it included a Shiga toxin 2 gene (stx(2)), two genes on the EHEC plasmid (toxB and ehxA), and the gene encoding intimin (eae). Despite the similarities, putative virulence genes distributed on O islands-large chromosomal DNA segments present in the O157:H7 genome-were useful for discriminating among STEC serotypes and the O121:H19 clone had a composite profile that was distinct from the profiles of the other major EHEC clones of pathogenic E. coli. On the basis of sequencing analysis with 13 housekeeping genes, the O121:H19 clone did not fall into any of the four classical EHEC and enteropathogenic E. coli groups but instead was closely related to two eae-negative STEC strains.

Adhesins, Bacterial↗

Deciphering the model pathogenic fungus Cryptococcus neoformans.

Cryptococcus neoformans is a basidiomycete fungal pathogen of humans that has diverged considerably from other model fungi such as Neurospora crassa, Aspergillus nidulans, Saccharomyces cerevisiae and the common human fungal pathogen Candida albicans. The recent completion of the genome sequences of two related C. neoformans strains and the ongoing genome sequencing of three other divergent Cryptococcus strains with different virulence phenotypes and environmental distributions should improve our understanding of this important pathogen. We discuss the biology of C. neoformans in light of this genomic data, with a special emphasis on the role that evolution and sexual reproduction have in the complex relationships of the fungus with the environment and the host.

Animals↗

[Serotypes and genotypes of dengue virus circulating in Venezuela, 1990-1997].

Due to the increasing severity of hemorrhagic dengue epidemics during the last years in Venezuela, a retrospective analysis was conducted to identify the behaviour of the dengue virus serotypes circulating in the country and the molecular evolution of dengue virus serotype 2. The data presented here indicates that dengue virus serotypes 1, 2 and 4 are endemic in Venezuela, they circulate simultaneously around the year in the biggest urban cities, however, one particular serotype is predominant during an epidemic period and replaces the virus serotype dominant during the previous epidemic period. The increased severity of dengue fever since 1989 in Venezuela might be associated to the introduction of the Asiatic genotype of virus which replaced the autochthonous Caribbean genotype. The Asiatic genotype is recognised as a more virulent virus.

Dengue↗

Diversity and specificity in the interaction between Caenorhabditis elegans and the pathogen Serratia marcescens.

BACKGROUND: Co-evolutionary arms races between parasites and hosts are considered to be of immense importance in the evolution of living organisms, potentially leading to highly dynamic life-history changes. The outcome of such arms races is in many cases thought to be determined by frequency dependent selection, which relies on genetic variation in host susceptibility and parasite virulence, and also genotype-specific interactions between host and parasite. Empirical evidence for these two prerequisites is scarce, however, especially for invertebrate hosts. We addressed this topic by analysing the interaction between natural isolates of the soil nematode Caenorhabditis elegans and the pathogenic soil bacterium Serratia marcescens. RESULTS: Our analysis reveals the presence of i) significant variation in host susceptibility, ii) significant variation in pathogen virulence, and iii) significant strain- and genotype-specific interactions between the two species. CONCLUSIONS: The results obtained support the previous notion that highly specific interactions between parasites and animal hosts are generally widespread. At least for C. elegans, the high specificity is observed among isolates from the same population, such that it may provide a basis for and/or represent the outcome of co-evolutionary adaptations under natural conditions. Since both C. elegans and S. marcescens permit comprehensive molecular analyses, these two species provide a promising model system for inference of the molecular basis of such highly specific interactions, which are as yet unexplored in invertebrate hosts.

Animals↗

The complete nucleotide sequence of a plant root-inducing (Ri) plasmid indicates its chimeric structure and evolutionary relationship between tumor-inducing (Ti) and symbiotic (Sym) plasmids in Rhizobiaceae.

The Ri (root-inducing) plasmid in Agrobacterium rhizogenes and Ti (tumor-inducing) plasmid in Agrobacterium tumefaciens have provided the fundamental basis for the construction of plant vectors and transgenic plants. Recently, the determination of the first complete nucleotide sequence of the Ti plasmid (pTi-SAKURA) has been successful. To understand the general structure of these oncogenic T-DNA transfer plasmids, the whole nucleotide sequence of a mikimopine-type Ri plasmid, pRi1724, was analyzed. The plasmid is 217,594 bp in size, and has 173 open reading frames (ORFs) in total, which are asymmetrically distributed. Except for 27 ORFs, which are unknown, 173 ORFs were classified into 12 groups as follows: three for DNA replication, nine for plasmid modification, 22 for conjugation, 26 for virulence, 11 for T-DNA gene, 19 for mikimopine/mikimopine-lactam transport, ten for an unknown opine metabolism, seven for transcriptional regulator, five for sugar transport, five for glycerol metabolism, four for chemoreceptor and 32 for others. The elucidated chimeric structure of pRi1724 interestingly indicates that the evolution of Rhizobiaceae plasmids seems to have kept interactions among the plasmids; especially, the genes and elements for a conjugal transfer of pRi1724 had clearly closer kinship to those of a Sym (symbiotic) plasmid, pNGR234a in Rhizobium sp. than those of Ti plasmids. By using sequencing and Northern analysis, we examined the metabolic pathway and gene expression of mikimopine, which is probably an Ri-specific opine.

ATP-Binding Cassette Transporters↗

[Antimicrobial resistance and bacterial virulence].

Hospitals are places with high selective pressure by antimicrobial agents. For this reason, bacteria producing nosocomial infections need to be not only virulent, but also resistant to antimicrobial agents. In the present review we analyse the effect of the acquisition of an antibiotic resistance phenotype in bacterial fitness and virulence. Besides that, we review as well the existence of common mechanisms for resistance to antimicrobial agents and bacterial virulence. In this line, we highlight the role of multidrug efflux pumps on bacterial virulence. Since opportunistic pathogens frequently have an environmental origin, we also discuss the role of natural ecosystems, as well as their potential contamination, on the selection of bacteria resistant to antimicrobial agents.

Animals↗

Conserved genes in a path from commensalism to pathogenicity: comparative phylogenetic profiles of Staphylococcus epidermidis RP62A and ATCC12228.

BACKGROUND: Staphylococcus epidermidis, long regarded as an innocuous commensal bacterium of the human skin, is the most frequent cause of nosocomial infections associated with implanted medical devices. This conditional pathogen provides a model of choice to study genome landmarks correlated with the transition between commensalism and pathogenicity. Traditional investigations stress differences in gene content. We focused on conserved genes that have accumulated small mutation differences during the transition. RESULTS: A comparison of strain ATCC12228, a non-biofilm forming, non-infection associated strain and strain RP62A, a methicillin-resistant biofilm clinical isolate, revealed consistent variation, mostly single-nucleotide polymorphisms (SNPs), in orthologous genes in addition to the previously investigated global changes in gene clusters. This polymorphism, scattered throughout the genome, may reveal genes that contribute to adaptation of the bacteria to different environmental stimuli, allowing them to shift from commensalism to pathogenicity. SNPs were detected in 931 pairs of orthologs with identical gene length, accounting for approximately 45% of the total pairs of orthologs. Assuming that non-synonymous mutations would mark recent evolution, and hence be associated to the onset of the pathogenic process, analysis of ratios of non-synonymous SNPs vs synonymous SNPs suggested hypotheses about possible pathogenicity determinants. The N/S ratios for virulence factors and surface proteins differed significantly from that of average SNPs. Of those gene pairs, 40 showed a disproportionate distribution of dN vs dS. Among those, the presence of the gene encoding methionine sulfoxide reductase suggested a possible involvement of reactive oxygen species. This led us to uncover that the infection associated strain was significantly more resistant to hydrogen peroxide and paraquat than the environmental strain. Some 16 genes of the list were of unknown function. We could suggest however that they were likely to belong to surface proteins or considered in priority as important for pathogenicity. CONCLUSION: Our study proposed a novel approach to identify genes involved in pathogenic processes and provided some insight about the molecular mechanisms leading a commensal inhabitant to become an invasive pathogen.

Bacterial Proteins↗

Very virulent infectious bursal disease virus: reduced pathogenicity in a rare natural segment-B-reassorted isolate.

The purpose of this study was to compare the molecular epidemiology of infectious bursal disease virus (IBDV) segments A and B of 50 natural or vaccine IBDV strains that were isolated or produced between 1972 and 2002 in 17 countries from four continents, with phenotypes ranging from attenuated to very virulent (vv). These strains were subjected to sequence and phylogenetic analysis based on partial sequences of genome segments A and B. Although there is co-evolution of the two genome segments (70 % of strains kept the same genetic relatives in the segment A- and B-defined consensus trees), several strains (26 %) were identified with the incongruence length difference test as exhibiting a significantly different phylogenetic relationship depending on which segment was analysed. This suggested that natural reassortment could have occurred. One of the possible naturally occurring reassortant strains, which exhibited a segment A related to the vvIBDV cluster whereas its segment B was not, was thoroughly sequenced (coding sequence of both segments) and submitted to a standardized experimental characterization of its acute pathogenicity. This strain induced significantly less mortality than typical vvIBDVs; however, the mechanisms for this reduced pathogenicity remain unknown, as no significant difference in the bursal lesions, post-infectious antibody response or virus production in the bursa was observed in challenged chickens.

Animals↗