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51 results for “Evolution of virulence”
A chromosome-level genome resource for studying virulence mechanisms and evolution of the coffee rust pathogen Hemileia vastatrix
<p>Recurrent epidemics of coffee leaf rust, caused by the fungal pathogen <em>Hemileia vastatrix,</em> have constrained the sustainable production of Arabica coffee for over 150 years. The ability of <em>H. vastatrix </em>to overcome resistance in coffee cultivars and evolve new races is inexplicable for a pathogen that supposedly only utilizes clonal reproduction. Understanding the evolutionary complexity between <em>H. vastatrix</em> and its only known host, including determining how the pathogen evolves virulence so rapidly is crucial for disease management. Achieving such goals relies on the availability of a comprehensive and high-quality genome reference assembly. To date, two reference genomes have been assembled and published for <em>H. vastatrix</em> that, while useful, remain fragmented and do not represent chromosomal scaffolds. Here, we present a complete scaffolded pseudochromosome-level genome resource for <em>H. vastatrix </em>strain 178a (Hv178a). Our initial assembly revealed an unusually high degree of gene duplication (over 50% BUSCO basidiomycota_odb10 genes). Upon inspection, this was predominantly due to a single scaffold that itself showed 91.9% BUSCO Completeness. Taxonomic analysis of predicted BUSCO genes placed this scaffold in Exobasidiomycetes and suggests it is a distinct genome, which we have named Hv178a associated fungal genome (Hv178a AFG). The high depth of coverage and close association with Hv178a raises the prospect of symbiosis, although we cannot completely rule out contamination at this time. The main Ca. 546 Mbp Hv178a genome was primarily (97.7%) localised to 11 pseudochromosomes (51.5 Mb N50), building the foundation for future advanced studies of genome structure and organization. Citation: https://doi.org/10.1101/2022.07.29.502101</p>
The effect of a temperature‐sensitive prophage on the evolution of virulence in an opportunistic bacterial pathogen
<p>Viruses are key actors of ecosystems and have major impacts on global biogeochemical cycles. Prophages deserve particular attention as they are ubiquitous in bacterial genomes and can enter a lytic cycle when triggered by environmental conditions. We explored how temperature affects the interactions between prophages and other biological levels by using an opportunistic pathogen, the bacterium <em>Serratia marcescens</em>, that harbours several prophages and that had undergone an evolution experiment under several temperature regimes. We found that the release of one of the prophages was temperature-sensitive and malleable to evolutionary changes. We further discovered that the virulence of the bacterium in an insect model also evolved and was positively correlated with phage release rates. We determined through analysis of genetic and epigenetic data that changes in the bacterial outer cell wall structure possibly explain this phenomenon. We hypothezise that the temperature-dependent phage release rate acted as a selection pressure on <em>S. marcescens</em> and that it resulted in modified bacterial virulence in the insect host. Our study system illustrates how viruses can mediate the influence of abiotic environmental changes to other biological levels and thus be involved in ecosystem feedback loops.</p>
Data from: Multispecies interactions and the community context of the evolution of virulence
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The effect of a temperature‐sensitive prophage on the evolution of virulence in an opportunistic bacterial pathogen
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Host heterogeneity mitigates virulence evolution
<p>Parasites often infect genetically diverse host populations, and the evolutionary trajectories of parasite populations may be shaped by levels of host heterogeneity. Mixed genotype host populations, compared to homogeneous host populations, can reduce parasite prevalence and potentially reduce rates of parasite adaptation due to tradeoffs associated with adapting to specific host genotypes. Here, we used experimental evolution to select for increased virulence in populations of the bacterial parasite <em>Serratia marcescens</em> exposed to either heterogenous or homogenous populations of<em> Caenorhabditis elegans</em>. We found that parasites exposed to heterogenous host populations evolved significantly less virulence than parasites exposed to homogeneous host populations over several hundred bacterial generations. Thus, host heterogeneity impeded parasite adaptation to host populations. While we detected tradeoffs in virulence evolution, parasite adaptation to two specific host genotypes also resulted in modestly increased virulence against the reciprocal host genotypes. These results suggest that parasite adaptation to heterogenous host populations may be impeded by both tradeoffs and a reduction in the efficacy of selection as different host genotypes exert different selective pressures on a parasite population.</p>
Data from: Incomplete host immunity favors the evolution of virulence in an emergent pathogen
Immune memory evolved to protect hosts from reinfection, but incomplete responses that allow future reinfection might inadvertently select for more harmful pathogens. We present empirical and modeling evidence that incomplete immunity promotes the evolution of higher virulence in a natural host-pathogen system. We performed sequential infections of house finches with Mycoplasma gallisepticum strains of varying virulence. Virulent bacterial strains generated stronger host protection against reinfection than less virulent strains, and thus excluded less virulent strains from infecting previously-exposed hosts. In a two-strain model, the resulting fitness advantage selected for an almost two-fold increase in pathogen virulence. Thus, the same immune systems that protect hosts from infection can concomitantly drive the evolution of more harmful pathogens in nature.
Complete telomere-to-telomere genomes uncover virulence evolution conferred by chromosome fusion in oomycete plant pathogens
<p><span>Variations in chromosome number are occasionally observed among oomycetes, a group that includes many plant pathogens, but the emergence of such variations and their effects on genome and virulence evolution remain ambiguous. We generated complete telomere-to-telomere genome assemblies for <em>Phytophthora sojae</em>, <em>Globisporangium ultimum</em>, <em>Pythium oligandrum</em>, and <em>G. spinosum</em>. Reconstructing the karyotype of the most recent common ancestor in Peronosporales revealed that frequent chromosome fusion and fission drove changes in chromosome number. Centromeres enriched with <em>Copia</em>-like transposons may contribute to chromosome fusion and fission events. Chromosome fusion facilitated the emergence of pathogenicity genes and their adaptive evolution. Effectors tended to duplicate in the sub-telomere regions of fused chromosomes, which exhibited evolutionary features distinct to the non-fused chromosomes. By integrating ancestral genomic dynamics and structural predictions, we have identified secreted Ankyrin repeat-containing proteins (ANKs) as a novel class of effectors in <em>P. sojae</em>. Phylogenetic analysis and experiments further revealed that ANK is a specifically expanded effector family in oomycetes. These results revealed chromosome dynamics in oomycete plant pathogens, and provided novel insights into karyotype and effector evolution.</span></p>
Host heterogeneity mitigates virulence evolution
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Data from: Incomplete host immunity favors the evolution of virulence in an emergent pathogen
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The evolution of virulence in Pseudomonas aeruginosa during chronic wound infection
<p>Opportunistic pathogens are associated with a number of chronic human infections, yet the evolution of virulence in these organisms during chronic infection remains poorly understood. Here, we tested the evolution of virulence in the human opportunistic pathogen Pseudomonas aeruginosa in a murine chronic wound model using a two-part serial passage and sepsis experiment, and found that virulence evolved in different directions in each line of evolution. We also assessed P. aeruginosa adaptation to a chronic wound after 42 days of evolution and found that morphological diversity in our evolved populations was limited compared to that previously described in cystic fibrosis (CF) infections. Using whole-genome sequencing, we found that genes previously implicated in P. aeruginosa pathogenesis (lasR, pilR, fleQ, rpoN and pvcA), contained mutations during the course of evolution in wounds, with selection occurring in parallel across all lines of evolution. Our findings highlight that (i) P. aeruginosa heterogeneity may be less extensive in chronic wounds than in CF lungs; (ii) genes involved in P. aeruginosa pathogenesis acquire mutations during chronic wound infection; (iii) similar genetic adaptations are employed by P. aeruginosa across multiple infection environments and (iv) current models of virulence may not adequately explain the diverging evolutionary trajectories observed in an opportunistic pathogen during chronic wound infection.</p>
Experimental evolution of virulence and associated traits in a Drosophila melanogaster – Wolbachia symbiosis
<p>Evolutionary theory predicts that vertically transmitted symbionts are selected for low virulence, as their fitness is directly correlated to that of their host. In contrast with this prediction, the <em>Wolbachia</em> strain <em>w</em>MelPop drastically reduces its <em>Drosophila melanogaster</em> host lifespan at high rearing temperatures. It is generally assumed that this feature is maintained because the <em>D. melanogaster</em>–<em>w</em>MelPop symbiosis is usually not exposed to environmental conditions in which the symbiont is virulent. To test this hypothesis, we submitted <em>w</em>MelPop-infected <em>D. melanogaster</em> lines to 17 generations of experimental evolution at a high temperature, while enforcing late reproduction. The fly survival was measured at different time points, as well as two traits that have been proposed to be causally responsible for <em>w</em>MelPop virulence: its relative density and the mean number of octomom copies present in its genome. We hypothesised that these conditions would select for a reduced <em>w</em>MelPop virulence, a reduced <em>w</em>MelPop density, and a reduced octomom copy number. Our results indicate that density, octomom copy number and virulence are correlated. However, contrary to our expectations, we could not detect any reduction in virulence during the course of evolution. We discuss the significance of our results with respect to the evolutionary causes of <em>w</em>MelPop virulence and propose that intra-host selection could explain this conundrum.</p>
Data from: How parasite interaction strategies alter virulence evolution in multi-parasite communities
The majority of organisms host multiple parasite species, each of which can interact with hosts and competitors through a diverse range of direct and indirect mechanisms. These within-host interactions can directly alter the mortality rate of coinfected hosts and alter the evolution of virulence (parasite induced host mortality). Yet we still know little about how within-host interactions affect the evolution of parasite virulence in multi-parasite communities. Here, we modeled the virulence evolution of two coinfecting parasites in a host population in which parasites interacted through cross immunity, immune suppression, immunopathology, or spite. We show (1) that these within-host interactions have different effects on virulence evolution when all parasites interact with each other in the same way vs. when coinfecting parasites have unique interaction strategies, (2) that all of these interactions cause the evolution of lower virulence in some hosts, and higher virulence in other hosts, depending on the hosts infection status, and (3) that for cross immunity and spite, whether parasites increased or decreased the evolutionarily stable virulence in coinfected hosts depended on interaction strength. These results improve our understanding of virulence evolution in complex parasite communities, and show that virulence evolution must be understood at the community scale.
Data from: Contrasting evolution of virulence and replication rate in an emerging bacterial pathogen
Host resistance through immune clearance is predicted to favour pathogens that are able to transmit faster and are hence more virulent. Increasing pathogen virulence is, in turn, typically assumed to be mediated by increasing replication rates. However, experiments designed to test how pathogen virulence and replication rates evolve in response to increasing host resistance, as well as the relationship between the two, are rare and lacking for naturally-evolving host-pathogen interactions. We inoculated 55 isolates of Mycoplasma gallisepticum collected over 20 years from outbreak, into house finches (Haemorhous mexicanus) from disease-unexposed populations, which have not evolved protective immunity to M. gallisepticum. We show using three different metrics of virulence (body mass loss, symptom severity and putative mortality rate) that virulence has increased linearly over >150,000 bacterial generations since outbreak (1994-2015). By contrast, while replication rates increased from outbreak through to the initial spread of resistance (1994-2004), no further increases have occurred subsequently (2007-2015). Finally, as a consequence, we found that any potential mediating effect of replication rate on virulence evolution was restricted to the period when host resistance was initially increasing in the population. Taken together, our results show that pathogen virulence and replication rates can evolve independently, particularly after the initial spread of host resistance. We hypothesize that the evolution of pathogen virulence can be driven primarily by processes such as immune manipulation after resistance spreads in host populations.
Data from: Abiotic environmental variation drives virulence evolution in a fish host-parasite geographic mosaic
1.Parasite virulence varies greatly. Theory predicts that this arises from parasites optimising a trade-off between the mortality they inflict on current hosts, and their transmission to future hosts. The effect of the environment on this coevolution is rarely considered. 2.Geographic mosaics are fertile systems for studying coevolution, but again, the diversity of outcomes is often assumed to result from co-evolutionary dynamism, rather than being moulded by the environment. 3.Here we quantify variation in virulence among lakes in a geographic mosaic of coevolution between a trematode ectoparasite (Gyrodactylus arcuatus) and its three-spined stickleback (Gasterosteus aculeatus) host. 4.Virulence varies greatly in this system, and parasites are generally locally adapted to their hosts. 5.Parasites are also locally adapted to the water in their own lake, and virulence is strongly related to lake pH, the dominant axis of abiotic environmental variation in this system. 6.These results suggest that the evolution of virulence can be substantially affected by the abiotic environment, which has important implications for understanding coevolution. There are also implications for the evolutionary management of disease e.g. ectoparasites in aquaculture, the impacts of which might be expected to reduce given ongoing acidification of aquatic ecosystems.
Vaccine driven virulence evolution: Consequences of unbalanced reductions in mortality and transmission and implications for pertussis vaccines
<p>Many vaccines have heterogenous effects across individuals. Additionally, some vaccines do not prevent infection, but reduce disease-associated mortality and transmission. Both of these factors will alter selection pressures on pathogens, and thus shape the evolution of pathogen virulence. We use a mathematical modeling framework to show that 1. the balance of how vaccines reduce transmission vs. mortality, and 2. individual variability in protection conferred, both shape the evolution of pathogen virulence. Epidemiological (burden of disease) and evolutionary (pathogen virulence) outcomes are both worse when vaccines confer smaller reductions in transmission than mortality. Furthermore, outcomes are modulated by variability in vaccine effects, with increased variability limiting the extent of virulence evolution but in some cases preventing eradication. These findings are pertinent to current concerns about the global resurgence of pertussis and the efficacy of pertussis vaccines, as the two classes of these vaccines may reduce disease symptoms without preventing infection and differ in their ability to reduce transmission. Furthermore, these findings point to the importance of generating precise predictions for virulence evolution in <i>B. pertussis </i>(and other similar pathogens) by incorporating empirical characterizations of vaccine effects into models capturing the epidemiological details of this system.</p>
Higher phage virulence accelerates the evolution of host resistance
<p>Pathogens vary strikingly in their virulence and the selection they impose on their hosts. While the evolution of different virulence levels is well studied, the evolution of host resistance in response to different virulence levels is less understood and as of now mainly based on observations and theoretical predictions with few experimental tests. Increased virulence can increase selection for host resistance evolution if resistance costs are outweighed by the benefits of avoiding infection. To test this, we experimentally evolved the bacterium <em>Vibrio alginolyticus</em> in the presence of two variants of a filamentous phage that differ in their virulence. The bacterial host exhibited two alternative defence strategies: (1) super infection exclusion (SIE) whereby phage-infected cells were immune to subsequent infection at a cost of reduced growth, and (2) surface receptor mutations (SRM) providing resistance to infection by preventing phage attachment. While SIE emerged rapidly against both phages, SRM evolved faster against the high compared to the low virulence phage. Using a mathematical model of our system we show that increasing virulence strengthens selection for SRM due to the higher costs of infection suffered by SIE immune hosts. Thus, by accelerating the evolution of host resistance, more virulent phages caused shorter epidemics.</p>
Data & codes for: Evolution of virulence in emerging epidemics: from theory to experimental evolution and back
<p>Data & Codes for:</p> <p><strong>Evolution of virulence in emerging epidemics: from theory to experimental evolution and back</strong><br><em>Wakinyan Benhamou, François Blanquart, Marc Choisy, Thomas W. Berngruber, Rémi Choquet and Sylvain Gandon</em></p> <p>___________________________________________________________________________________</p> <p>Data that were used in this study, along with the scripts for the analyses (in R), are available in the file <strong><em>Data_and_codes.zip</em></strong><em>. </em>For full description, please see the file <strong><em>README.md</em></strong>. All this is also available in the following GitHub repositery: <a href="https://github.com/WakinyanB/LAMBDA">https://github.com/WakinyanB/LAMBDA</a>.</p>
The evolution of virulence in Pseudomonas aeruginosa during chronic wound infection
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Data from: Abiotic environmental variation drives virulence evolution in a fish host-parasite geographic mosaic
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Vaccine driven virulence evolution: Consequences of unbalanced reductions in mortality and transmission and implications for pertussis vaccines
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