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56 results for “parasite virulence”
Double Trouble : Multiple infections and the coevolution of virulence-resistance in structured host-parasite populations - Scripts, Data and Supplementary Material
<p>Supplementary material</p> <p> </p> <p>Contains the Mathematica notebook for analytical and numerical computations, and figure generation.</p> <p>An Rscript used to reproduce the coevolutionary figures from section "Coevolution"</p> <p>The set of appendices in a .pdf file.</p>
Data from: Abiotic environmental variation drives virulence evolution in a fish host-parasite geographic mosaic
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Data from: Alternative paths to success in a parasite community: within-host competition can favor higher virulence or direct interference
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Data from: How parasite interaction strategies alter virulence evolution in multi-parasite communities
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Transcriptome-wide comparisons and virulence gene polymorphisms of host-associated genotypes of the cnidarian parasite Ceratonova shasta in salmonids
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Data from: Patterns of host-parasite adaptation in three populations of monarch butterflies infected with a naturally occurring protozoan disease: virulence, resistance, and tolerance
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Data from: Coevolution between mutualists and parasites in symbiotic communities may lead to the evolution of lower virulence
Most eukaryotes harbor a diverse community of parasitic, mutualistic and commensal microbial symbionts. Although the diversity of these microbial symbiotic communities has recently drawn considerable attention, theory regarding the evolution of interactions among symbionts and with the host is still in nascent stages. Here we evaluate the role of interactions among co-infecting symbionts in the evolution of symbiont virulence towards the host. To do so, we place the virulence-transmission trade-off into a community context and model the evolution of symbiont trophic modes along the continuum from parasitism (virulence) to mutualism (negative virulence). We establish a framework for studying multiple infections of a host by the same symbiont species, and co-infection by multiple species, using a concept of shared costs, wherein the negative consequences of virulence, or harm, toward the host are shared among symbionts. Our results show that mutualism can be maintained under infection by multiple symbionts when shared costs are sufficiently low, while greater virulence and parasitism toward the host are more likely when shared costs are high. Lastly, for co-infection by more than one species, we show that if the presence of a mutualist ameliorates some of the costs of pathogen virulence, then the symbiotic community may more often evolve to a more commensal state and maintain mutualisms.
Data from: Genetic diversity, virulence and fitness evolution in an obligate fungal parasite of bees
Within-host competition is predicted to drive the evolution of virulence in parasites, but the precise outcomes of such interactions are often unpredictable due to many factors including the biology of the host and the parasite, stochastic events and co-evolutionary interactions. Here, we use a serial passage experiment (SPE) with three strains of a heterothallic fungal parasite (Ascosphaera apis) of the Honey bee (Apis mellifera) to assess how evolving under increasing competitive pressure affects parasite virulence and fitness evolution. The results show an increase in virulence after successive generations of selection and consequently faster production of spores. This faster sporulation, however, did not translate into more spores being produced during this longer window of sporulation; rather, it appeared to induce a loss of fitness in terms of total spore production. There was no evidence to suggest that a greater diversity of competing strains was a driver of this increased virulence and subsequent fitness cost, but rather that strain-specific competitive interactions influenced the evolutionary outcomes of mixed infections. It is possible that the parasite may have evolved to avoid competition with multiple strains because of its heterothallic mode of reproduction, which highlights the importance of understanding parasite biology when predicting disease dynamics.
Data from: No immediate or future extra costs of raising a virulent brood parasite chick
Parental care is an adaptive behaviour increasing the survival of young. Virulent brood parasites, like the common cuckoo Cuculus canorus, avoid the parental care and leave the care for their nestlings to hosts. Although raising a cuckoo is always costly because it kills host's progeny, to date it is not known whether raising of a brood parasite itself represents an extra cost affecting host's fitness. We quantified costs of rearing a cuckoo nestling in the most frequent host, the reed warbler Acrocephalus scirpaceus. We measured changes in the host physical (body mass) and physiological conditions (stress levels quantified via heterophils/lymphocytes ratio) within the one breeding attempt (immediate cost) and re-trapped some of these adults in the next breeding season to estimate return rates as a measure of their survival (future cost). In contrast to universal claims in the literature, raising a cuckoo nestling did not entail any extra immediate or future costs for hosts. This counterintuitive result reconciles theoretical expectations in the hosts with surprisingly low levels of counter-defences, including the reed warbler. Unexpectedly low costs of parasitism may also explain a long-term maintenance of some host-parasite systems.
Data from: Limiting opportunities for cheating stabilizes virulence in insect parasitic nematodes
Cooperative secretion of virulence factors by pathogens can lead to social conflict when cheating mutants exploit collective secretion, but do not contribute to it. If cheats outcompete cooperators within hosts, this can cause loss of virulence. Insect parasitic nematodes are important biocontrol tools that secrete a range of significant virulence factors. Critically, effective nematodes are hard to maintain without live passage, which can lead to virulence attenuation. Using experimental evolution we tested whether social cheating might explain unstable virulence in the nematode Heterorhabditis floridensis by manipulating relatedness via multiplicity of infection (MOI), and the scale of competition. Passage at high MOI, which should reduce relatedness, led to loss of fitness: virulence and reproductive rate declined together and all eight independent lines suffered premature extinction. As theory predicts, relatedness treatments had more impact under stronger global competition. In contrast, low MOI passage led to more stable virulence and increased reproduction. Moreover, low MOI lineages showed a trade-off between virulence and reproduction, particularly for lines under stronger between-host competition. Overall, this study indicates that evolution of virulence theory is valuable for the culture of biocontrol agents: effective nematodes can be improved and maintained if passage methods mitigate possible social conflicts.
Data from: Mice infected with low-virulence strains of Toxoplasma gondii lose their innate aversion to cat urine, even after extensive parasite clearance
Toxoplasma gondii chronic infection in rodent secondary hosts has been reported to lead to a loss of innate, hard-wired fear toward cats, its primary host. However the generality of this response across T. gondii strains and the underlying mechanism for this pathogen-mediated behavioral change remain unknown. To begin exploring these questions, we evaluated the effects of infection with two previously uninvestigated isolates from the three major North American clonal lineages of T. gondii, Type III and an attenuated strain of Type I. Using an hour-long open field activity assay optimized for this purpose, we measured mouse aversion toward predator and non-predator urines. We show that loss of innate aversion of cat urine is a general trait caused by infection with any of the three major clonal lineages of parasite. Surprisingly, we found that infection with the attenuated Type I parasite results in sustained loss of aversion at times post infection when neither parasite nor ongoing brain inflammation were detectable. This suggests that T. gondii-mediated interruption of mouse innate aversion toward cat urine may occur during early acute infection in a permanent manner, not requiring persistence of parasite cysts or continuing brain inflammation.
Data from: Within-host competition in genetically diverse malaria infections: parasite virulence and competitive success.
Humans and animals often become coinfected with pathogen strains that differ in virulence. The ensuing interaction between these strains can, in theory, be a major determinant of the direction of selection on virulence genes in pathogen populations. Many mathematical analyses of this assume that virulent pathogen lineages have a competitive advantage within coinfected hosts and thus predict that pathogens will evolve to become more virulent where genetically diverse infections are common. Although the implications of these studies are relevant to both fundamental biology and medical science, direct empirical tests for relationships between virulence and competitive ability are lacking. Here we use newly developed strain-specific real-time quantitative polymerase chain reaction protocols to determine the pairwise competitiveness of genetically divergent Plasmodium chabaudi clones that represent a wide range of innate virulences in their rodent host. We found that even against their background of widely varying genotypic and antigenic properties, virulent clones had a competitive advantage in the acute phase of mixed infections. The more virulent a clone was relative to its competitor, the less it suffered from competition. This result confirms our earlier work with parasite lines derived from a single clonal lineage by serial passage and supports the virulence-competitive ability assumption of many theoretical models. To the extent that our rodent model captures the essence of the natural history of malaria parasites, public health interventions which reduce the incidence of mixed malaria infections should have beneficial consequences by reducing the selection for high virulence.
Data from: Minor environmental concentrations of antibiotics can modify bacterial virulence in co-infection with a non-targeted parasite
Leakage of medical residues into the environment can significantly impact natural communities. For example, antibiotic contamination from agriculture and aquaculture can directly influence targeted pathogens, but also other non-targeted taxa of commensals and parasites that regularly co-occur and co-infect the same host. Consequently, antibiotics could significantly alter interspecific interactions and epidemiology of the co-infecting parasite community. We studied how minor environmental concentration of antibiotic affects the coinfection of two parasites, the bacterium Flavobacterium columnare and the fluke Diplostomum pseudospathaceum, in their fish host. We found that antibiotic in feed, and particularly the minute concentration in water, significantly decreased bacterial virulence and changed the infection success of the flukes. These effects depended on the level of antibiotic resistance of the bacterial strains. Antibiotic, however, did not compensate for the higher virulence of co-infections. Our results demonstrate that even very low environmental concentration of antibiotic can influence ecology and epidemiology of diseases in co-infection with non-targeted parasites. Leakage of antibiotics into the environment may thus have more complex effects on disease ecology than previously anticipated.
Fig. 6 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system
Fig. 6. Log fold change in immunogloblulin expression relative to controls on day 14 in intestine samples. Parasite copy numbers measured in intestine samples are overlaid on IgM intestine plot (parasite copy number data are the same for the IgT plot). Letters denote treatments that differed (Tukey's HSD tests, α = 0.05).
Fig. 5 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system
Fig. 5. Log-foldchange in cytokine expression relative to controls at day-14 in spleen and intestine samples. Parasite copy numbers measured in gill tissues is overlaid on IFN-gamma spleen plot and parasite copy numbers measured in intestine samples are overlaid on IFN-gamma intestine plot, but parasite copy number data are the same for, and apply to, all cytokine plots underneath. Letters denote treatments that differed (Tukey's HDS tests, α = 0.05).
Data from: Mice infected with low-virulence strains of Toxoplasma gondii lose their innate aversion to cat urine, even after extensive parasite clearance
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Data from: The genome of the yellow potato cyst nematode Globodera rostochiensis reveals insights into the basis of parasitism and virulence
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Data from: Superinfection and the coevolution of parasite virulence and host recovery
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Data from: Genetic diversity, virulence and fitness evolution in an obligate fungal parasite of bees
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Data from: Within-host competition in genetically diverse malaria infections: parasite virulence and competitive success.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
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