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PubMed2001

Epidemiology, evolution, and future of the HIV/AIDS pandemic.

We used mathematical models to address several questions concerning the epidemiologic and evolutionary future of HIV/AIDS in human populations. Our analysis suggests that 1) when HIV first enters a human population, and for many subsequent years, the epidemic is driven by early transmissions, possibly occurring before donors have seroconverted to HIV-positive status; 2) new HIV infections in a subpopulation (risk group) may decline or level off due to the saturation of the susceptible hosts rather than to evolution of the virus or to the efficacy of intervention, education, and public health measures; 3) evolution in humans for resistance to HIV infection or for the infection to engender a lower death rate will require thousands of years and will be achieved only after vast numbers of persons die of AIDS; 4) evolution is unlikely to increase the virulence of HIV; and 5) if HIV chemotherapy reduces the transmissibility of the virus, treating individual patients can reduce the frequency of HIV infections and AIDS deaths in the general population.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Genetic characterization of pathogenic Saccharomyces cerevisiae isolates.

Saccharomyces cerevisiae isolates from human patients have been genetically analyzed. Some of the characteristics of these isolates are very different from laboratory and industrial strains of S. cerevisiae and, for this reason, stringent genetic tests have been used to confirm their identity as S. cerevisiae. Most of these clinical isolates are able to grow at 42 degrees, a temperature that completely inhibits the growth of most other S. cerevisiae strains. This property can be considered a virulence trait and may help explain the presence of these isolates in human hosts. The ability to grow at 42 degrees is shown to be polygenic with primarily additive effects between loci. S. cerevisiae will be a useful model for the evolution and genetic analysis of fungal virulence and the study of polygenic traits.

Crosses, Genetic↗
PubMed2000

Acquisition of multiple virulence/avirulence determinants by potato virus X (PVX) has occurred through convergent evolution rather than through recombination.

Resistance to potato virus X (PVX) is determined by the product of a host resistance gene and a viral determinant specifying either virulence (resistance-breaking ability) or avirulence (resistance sensitivity). The viral coat protein is the determinant of resistance mediated by the host Nx gene while the 25 kDa movement protein is the determinant of Nb-mediated resistance. Group 1 and group 4 strains of PVX are avirulent or virulent respectively for both these determinants while group 2 and group 3 strains are virulent for one but avirulent for the other determinant. There are two alternative evolutionary mechanisms by which the various strain groups might have evolved: either by recombination between strains carrying virulence (or avirulence) determinants that evolved once only, or alternatively, by independent evolution of at least one virulence (or avirulence) determinant in distinct phylogenetic branches. These alternative hypotheses were investigated by (i) determining the complete genomic sequence of a group 1 and a group 4 strain and (ii) comparing the completely sequenced genomes of six isolates representative of the four strain groups. The analysis revealed the same phylogeny for all five PVX genes. Thus, there is no evidence that the PVX strain groups evolved by recombination.

5' Untranslated Regions↗
PubMed1994

Chance and selection in the evolution of barley mildew.

Populations of the barley powdery mildew fungus are genetically very diverse. However, when a new resistance gene is introduced into barley to control mildew, the population of the pathogen may respond by rapid growth of a few virulent clones. These phases of rapid clonal evolution cause radical changes in the frequencies of mildew genotypes.

Biological Evolution↗
PubMed2002

Mating-type locus of Cryptococcus neoformans: a step in the evolution of sex chromosomes.

The sexual development and virulence of the fungal pathogen Cryptococcus neoformans is controlled by a bipolar mating system determined by a single locus that exists in two alleles, alpha and a. The alpha and a mating-type alleles from two divergent varieties were cloned and sequenced. The C. neoformans mating-type locus is unique, spans >100 kb, and contains more than 20 genes. MAT-encoded products include homologs of regulators of sexual development in other fungi, pheromone and pheromone receptors, divergent components of a MAP kinase cascade, and other proteins with no obvious function in mating. The alpha and a alleles of the mating-type locus have extensively rearranged during evolution and strain divergence but are stable during genetic crosses and in the population. The C. neoformans mating-type locus is strikingly different from the other known fungal mating-type loci, sharing features with the self-incompatibility systems and sex chromosomes of algae, plants, and animals. Our study establishes a new paradigm for mating-type loci in fungi with implications for the evolution of cell identity and self/nonself recognition.

Alleles↗
PubMed2006

Cooperation and virulence in acute Pseudomonas aeruginosa infections.

BACKGROUND: Efficient host exploitation by parasites is frequently likely to depend on cooperative behaviour. Under these conditions, mixed-strain infections are predicted to show lower virulence (host mortality) than are single-clone infections, due to competition favouring non-contributing social 'cheats' whose presence will reduce within-host growth. We tested this hypothesis using the cooperative production of iron-scavenging siderophores by the pathogenic bacterium Pseudomonas aeruginosa in an insect host. RESULTS: We found that infection by siderophore-producing bacteria (cooperators) results in more rapid host death than does infection by non-producers (cheats), and that mixtures of both result in intermediate levels of virulence. Within-host bacterial growth rates exhibited the same pattern. Crucially, cheats were more successful in mixed infections compared with single-clone infections, while the opposite was true of cooperators. CONCLUSION: These data demonstrate that mixed clone infections can favour the evolution of social cheats, and thus decrease virulence when parasite growth is dependent on cooperative behaviours.

Animals↗
PubMed2005

Diversification of transmission modes and the evolution of mutualism.

In order for mutualism to evolve, some force must align the interests of the two interacting partners. Vertical transmission can fill this role, but it is still unknown whether mutualism can be stable when vertically transmitted symbionts can evolve toward horizontal transmission. In this article, we investigate how symbionts' transmission mode and virulence should evolve, depending on the relationship between these two traits. We show that pathogens that reduce their host's fecundity can have more complex evolutionary dynamics than those that increase mortality. In some cases, runaway evolution of virulence can drive the host population extinct. In most cases, evolutionary branching results in the differentiation of avirulent, vertically transmitted symbionts from virulent, contagious pathogens. The population of symbionts then becomes polymorphic, and because the least virulent symbionts are the most frequent, the average virulence of symbionts is much lower than it would be in a monomorphic population. When the link between transmission and virulence results from correlated mutational changes and not from fixed constraints, vertically transmitted symbionts do not simply lose virulence; they evolve toward mutualism. We show that the force that stabilizes mutualism in such situations is the competition for transmission between symbionts.

Evolution, Molecular↗
PubMed2002

Escherichia coli in disguise: molecular origins of Shigella.

Shigella, which still stands as a genus with four species today, in reality belongs to the extremely diverse species Escherichia coli. There are several lineages of Shigella strains derived through independent acquisition of the pINV virulence plasmid. The chromosomally determined phenotypic properties of Shigella result from convergent evolution during niche adaptation, most due to loss of function, some from negative selection pressure.

Adaptation, Biological↗
PubMed1997

[Genes involved in the virulence of enterohemorrhagic Escherichia coli].

Some of the virulent genes of enterohemorrhagic E. coli(EHEC) are described. stx, bfpA, eaeA and ehxA encode an enterocytotoxin homologous to Shiga toxin, bundle-forming pilus, intimin and an RTX toxin, respectively. In pathogenesis, although bfp and eae cause diarrhea, and ehx and stx seem to cause hemorrhagic colitis and hemolytic uremic syndrome, many problems remain for prevention and treatment of these symptoms. In evolution, it is intriguining that the virulent genes of EHEC might be mediated by phages, plasmids and so on, because stx is derived from a bacterio-phage, bfpA is located in a plasmid in enteropathogenic E. coli(EPEC) though it has not yet been cloned in EHEC, eaeA is one of the genes in LEE(locus of enterocyte effacement), a putative genetic cassette ubiquitous for EPEC and EHEC, and ehxA is in a plasmid.

Adhesins, Escherichia coli↗
PubMed2004

Cooperation and competition in pathogenic bacteria.

Explaining altruistic cooperation is one of the greatest challenges for evolutionary biology. One solution to this problem is if costly cooperative behaviours are directed towards relatives. This idea of kin selection has been hugely influential and applied widely from microorganisms to vertebrates. However, a problem arises if there is local competition for resources, because this leads to competition between relatives, reducing selection for cooperation. Here we use an experimental evolution approach to test the effect of the scale of competition, and how it interacts with relatedness. The cooperative trait that we examine is the production of siderophores, iron-scavenging agents, in the pathogenic bacterium Pseudomonas aeruginosa. As expected, our results show that higher levels of cooperative siderophore production evolve in the higher relatedness treatments. However, our results also show that more local competition selects for lower levels of siderophore production and that there is a significant interaction between relatedness and the scale of competition, with relatedness having less effect when the scale of competition is more local. More generally, the scale of competition is likely to be of particular importance for the evolution of cooperation in microorganisms, and also the virulence of pathogenic microorganisms, because cooperative traits such as siderophore production have an important role in determining virulence.

Altruism↗
PubMed2006

Understanding the rise of the superbug: investigation of the evolution and genomic variation of Staphylococcus aureus.

The bacterium Staphylococcus aureus is a common cause of human infection, and it is becoming increasingly virulent and resistant to antibiotics. Our understanding of the evolution of this species has been greatly enhanced by the recent sequencing of the genomes of seven strains of S. aureus. Comparative genomic analysis allows us to identify variation in the chromosomes and understand the mechanisms by which this versatile bacterium has accumulated diversity within its genome structure.

Drug Resistance↗
PubMed2004

Helicobacter acinonychis: genetic and rodent infection studies of a Helicobacter pylori-like gastric pathogen of cheetahs and other big cats.

Insights into bacterium-host interactions and genome evolution can emerge from comparisons among related species. Here we studied Helicobacter acinonychis (formerly H. acinonyx), a species closely related to the human gastric pathogen Helicobacter pylori. Two groups of strains were identified by randomly amplified polymorphic DNA fingerprinting and gene sequencing: one group from six cheetahs in a U.S. zoo and two lions in a European circus, and the other group from a tiger and a lion-tiger hybrid in the same circus. PCR and DNA sequencing showed that each strain lacked the cag pathogenicity island and contained a degenerate vacuolating cytotoxin (vacA) gene. Analyses of nine other genes (glmM, recA, hp519, glr, cysS, ppa, flaB, flaA, and atpA) revealed a approximately 2% base substitution difference, on average, between the two H. acinonychis groups and a approximately 8% difference between these genes and their homologs in H. pylori reference strains such as 26695. H. acinonychis derivatives that could chronically infect mice were selected and were found to be capable of persistent mixed infection with certain H. pylori strains. Several variants, due variously to recombination or new mutation, were found after 2 months of mixed infection. H. acinonychis ' modest genetic distance from H. pylori, its ability to infect mice, and its ability to coexist and recombine with certain H. pylori strains in vivo should be useful in studies of Helicobacter infection and virulence mechanisms and studies of genome evolution.

Acinonyx↗
PubMed2004

The SRS superfamily of Toxoplasma surface proteins.

The surface of the protozoan parasite Toxoplasma gondii is coated with developmentally expressed, glycosylphosphatidylinositol-linked proteins structurally related to the highly immunogenic surface antigen SAG1. Collectively, these surface antigens are known as the SRS (SAG1-related sequences) superfamily of proteins. SRS proteins are thought to mediate attachment to host cells and activate host immunity to regulate the parasite's virulence. To better understand the number, evolution and developmental expression of SRS genes, this study has bioinformatically identified 161 unique SRS DNA sequences present in the T. gondii type II Me49 genome. The SRS superfamily of sequences phylogenetically bifurcates into two subfamilies, the prototypic members being SAG1 and SAG2A, respectively. Paralogous SRS sequences are 24-99% identical, are tandemly arrayed throughout the genome, and are present on most, if not all, chromosomes. All 11 SRS sequences on chromosomes Ia and Ib are clustered at sub-telomeric expression sites. Messenger RNA expression in the majority of SRS sequences for which multiple Expressed Sequence Tags exist is developmentally regulated. A consensus nucleotide sequence surrounding both the splice acceptor and donor sites was identified in those SRS sequences possessing an intron. Genotypic differences among SRS sequences are present at several loci (e.g. the absence of SAG5B, the truncation of SAG2D in Me49 compared with RH) indicating that different genotypes possess distinct sets of SRS sequences. Orthologous genes are restricted to tissue-dwelling coccidia (Neospora, Sarcocystis) with no related sequences present in other more distant apicomplexa such as Eimeria, Cryptosporidia, and Plasmodium spp.

Animals↗
PubMed2004

Fitness of Toxoplasma gondii is not related to DHFR single-nucleotide polymorphism during congenital toxoplasmosis.

Factors that regulate the pathogenesis of Toxoplasma gondii in humans are poorly understood. When acquired during pregnancy, toxoplasmosis can be disastrous, leading to fetal loss or conversely to subclinical disease. In congenitally infected infants, evolution is highly unpredictable. Genotype based virulence patterns have been described in mice, but in humans this classification does not correlate with the gravity of the disease. Mutations on DHFR-TS loci have recently been reported to confer T. gondii fitness cost. In this study, we investigated the relationship between the virulence of the parasite, as measured by clinical outcome in the fetus or newborn, fitness, as measured by parasitic load in amniotic fluid, and allelic polymorphism in DHFR. Six cases of severe congenital toxoplasmosis and 23 cases of mild congenital infections were included in the study. Quantitative PCR was performed to evaluate total T. gondii DNA load in amniotic fluid and detection of mutations was carried out with a LightCycler using hybridisation probes. Parasitic load was significantly higher in severe infections than in mild diseases. Among isolates from severe or non-severe cases of congenital toxoplasmosis, no polymorphism could be detected at loci 36, 83 or 245 of the DHFR gene. The virulent RH strain presented the same melting temperature as the non-virulent PRU strain for codons 36, 83 and 245. Only mutated clones, M2M3 and M2M4 with allelic replacement at these positions, displayed different profiles allowing a clear distinction between wild and mutant types. We concluded that the DHFR gene mutations we investigated do not regulate T. gondii fitness in humans.

Animals↗
PubMed2001

Ancestral divergence, genome diversification, and phylogeographic variation in subpopulations of sorbitol-negative, beta-glucuronidase-negative enterohemorrhagic Escherichia coli O157.

The O157:H7 lineage of enterohemorrhagic Escherichia coli is a geographically disseminated complex of highly related genotypes that share common ancestry. The common clone that is found worldwide carries several markers of events in its evolution, including markers for acquisition of virulence genes and loss of physiological characteristics, such as sorbitol fermentation ability and beta-glucuronidase production. Populations of variants that are distinct with respect to motility and the sorbitol and beta-glucuronidase markers appear to have diverged at several points along the inferred evolutionary pathway. In addition to these variants, distinct subpopulations of the contemporary non-sorbitol-fermenting, beta-glucuronidase-negative O157:H7 clone were recently detected among bovine and human clinical isolates in the United States by using high-resolution genome comparison. In order to determine if these recently described subpopulations were derived from a regional or ancestral divergence event, we used octamer-based genome scanning, marker sorting, and DNA sequence analysis to examine their phylogenetic relationship to populations of non-sorbitol-fermenting, beta-glucuronidase negative O157:H7 and O157:H- strains from Australia. The inferred phylogeny is consistent with the hypothesis that subpopulations on each continent resulted from geographic spread of an ancestral divergence event and subsequent expansion of distinct subpopulations. Marker sorting and DNA sequence analyses identified sets of monophyletic markers consistent with the pattern of divergence and demonstrated that phylogeographic variation occurred through emergence of regional subclones and concentration of regional polymorphisms among distinct subpopulations. DNA sequence analysis of representative polyphyletic markers showed that genome diversity accrued through random drift and bacteriophage-mediated events.

Animals↗
PubMed2002

Evolution of replication efficiency following infection with a molecularly cloned feline immunodeficiency virus of low virulence.

The development of an effective vaccine against human immunodeficiency virus is considered to be the most practicable means of controlling the advancing global AIDS epidemic. Studies with the domestic cat have demonstrated that vaccinal immunity to infection can be induced against feline immunodeficiency virus (FIV); however, protection is largely restricted to laboratory strains of FIV and does not extend to primary strains of the virus. We compared the pathogenicity of two prototypic vaccine challenge strains of FIV derived from molecular clones; the laboratory strain PET(F14) and the primary strain GL8(414). PET(F14) established a low viral load and had no effect on CD4(+)- or CD8(+)-lymphocyte subsets. In contrast, GL8(414) established a high viral load and induced a significant reduction in the ratio of CD4(+) to CD8(+) lymphocytes by 15 weeks postinfection, suggesting that PET(F14) may be a low-virulence-challenge virus. However, during long-term monitoring of the PET(F14)-infected cats, we observed the emergence of variant viruses in two of three cats. Concomitant with the appearance of the variant viruses, designated 627(W135) and 628(W135,) we observed an expansion of CD8(+)-lymphocyte subpopulations expressing reduced CD8 beta-chain, a phenotype consistent with activation. The variant viruses both carried mutations that reduced the net charge of the V3 loop (K409Q and K409E), giving rise to a reduced ability of the Env proteins to both induce fusion and to establish productive infection in CXCR4-expressing cells. Further, following subsequent challenge of naïve cats with the mutant viruses, the viruses established higher viral loads and induced more marked alterations in CD8(+)-lymphocyte subpopulations than did the parent F14 strain of virus, suggesting that the E409K mutation in the PET(F14) strain contributes to the attenuation of the virus.

Amino Acid Sequence↗