Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
56
datasets available to search
ShareScore release 0.9.0
Dataset results
56 results for “parasite virulence”
Diffraction images used to solve the structures published in the article "A Family of Dual-Activity Glycosyltransferase-Phosphorylases Mediates Mannogen Turnover and Virulence in Leishmania Parasites"
<p>Raw diffraction images used for generating the structures published in the article A Family of Dual-Activity Glycosyltransferase-Phosphorylases Mediates Mannogen Turnover and Virulence in Leishmania Parasites" (available <a href="https://doi.org/10.1016/j.chom.2019.08.009">here</a>). The software used for the processing of each dataset is listed in their respective PDB entries.</p> <p> </p> <p>If you find this useful, please contact me at <a href="mailto:lukasz.sobala@hirszfeld.pl">lukasz.sobala@hirszfeld.pl</a>, I am just interested in how these data are used!</p>
Phenotypic data related to genetic architecture of transmission stage production and virulence in schistosome parasites
<p>These data were generated related to the study of the <strong>Genetic architecture of transmission stage production and virulence in schistosome parasites</strong>.</p> <p><strong>Abstract:</strong> Both theory and experimental data from multiple pathogens suggest that the production of transmission stages should be strongly associated with virulence, but the genetic bases of parasite transmission/virulence traits are poorly understood. In the blood fluke <em>Schistosoma mansoni</em>, parasite genotypes show extensive variation in numbers of cercariae larvae shed from infected snails. Furthermore, high shedding parasites cause high mortality to snails while low shedding parasites cause low mortality, consistent with expected trade-offs between parasite transmission and virulence. To understand the genetic basis of transmission stage production/virulence, we conducted reciprocal crosses between schistosomes from two laboratory populations that differ 8-fold in cercarial shedding and in their virulence to inbred snail hosts. Each parasite generation, we determined four-week cercarial shedding profiles in inbred <em>Biomphalaria glabrata</em> snails infected with single parasite larvae. We sequenced the whole genome of the F0 parents and the exome of the F1 progeny and 188 F2 progeny from each cross, and used linkage mapping to reveal quantitative trait loci (QTLs) underlying transmission stage production. Cercarial production is polygenic: we found three major QTLs on chromosome 1, 3 and 5 (Log-of-the-odds (LOD) = 5.61, 8.19, 6.25) and two minor QTLs on chromosome 2 and 4. These QTLs act additively and explained 28.56% of the phenotypic variation in cercarial shedding. Alleles inherited from the high and low shedding parents were co-dominant at all QTLs, except for chr. 1 and chr. 4 where the “high cercarial shedding” allele is recessive. These results demonstrate that the genetic architecture of key traits directly relevant to schistosome ecology can be dissected using classical linkage mapping approaches, and set the stage for fine mapping and functional validation of the genes involved using the growing armory of functional and cell biology tools available for this parasite.</p> <p> </p> <p>This dataset is made of 4 tables:</p> <ul> <li>F0_parental_populations.csv</li> <li>F1.csv</li> <li>F2.csv</li> <li>sex.tsv</li> </ul> <p> </p> <p><strong>F0_parental_populations.csv</strong></p> <p> </p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of <em>Schistosoma mansoni</em> parasite. We have compared the transmission stage production between two different populations of <em>S. mansoni</em> parasite. This dataset was originally published in Le Clec'h et al., 2019 (Striking differences in virulence, transmission and sporocyst growth dynamics between two schistosome populations. Parasites and Vectors. 2019 Oct 16;12(1):485. doi: 10.1186/s13071-019-3741-z).</p> <p> </p> <p>This table is made of 9 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>schistosoma_population</strong>: the population of schistosome used for the infection of the snail. Each snail was infected with a single parasite genotype. We have used SmLE (high shedder/highly virulent population) and SmBRE (low shedding/low virulent population).</li> <li><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4).</li> <li><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined by PCR <sup>1</sup>.</li> </ul> <p> </p> <p><strong>F1.csv</strong></p> <p> </p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of F1 progeny from the cross SmLE x SmBRE (see the manuscript for details).</p> <p> </p> <p>This table is made of 11 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>cross</strong>: F1A or F1B cross. Each snail was infected with a single parasite genotype from either F1A or F1B progeny.</li> <li><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4).</li> <li><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>PO</strong>: the total phenoloxidase activity in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>2</sup>.</li> <li><strong>Hb</strong>: the hemoglobin rate in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>3</sup>.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined by PCR <sup>1</sup>.</li> </ul> <p> </p> <p><strong>F2.csv</strong></p> <p>This table contains the number of cercariae produced by each individual <em>Biomphalaria glabrata</em> Bg26 snails infected with single genotypes of F2 progeny from the cross SmLE x SmBRE (see the manuscript for details).</p> <p> </p> <p>This table is made of 10 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample.</li> <li><strong>cross</strong>: F2A or F2B cross. Each snail was infected with a single parasite genotype from either F2A or F2B progeny.</li> <li><strong>Shed.1</strong>: the number of cercariae produced by each parasite genotype at the first shedding week (4 weeks after exposure to parasite).</li> <li><strong>Shed.2</strong>: the number of cercariae produced by each parasite genotype at the second shedding week (5 weeks after exposure to parasite).</li> <li><strong>Shed.3</strong>: the number of cercariae produced by each parasite genotype at the third shedding week (6 weeks after exposure to parasite).</li> <li><strong>Shed.4</strong>: the number of cercariae produced by each parasite genotype at the fourth shedding week (7 weeks after exposure to parasite).</li> <li><strong>sum</strong>: the sum of the cercariae produced by each parasite genotype over the 4 weeks of shedding (Shed.1 + Shed.2 + Shed.3 + Shed.4)</li> <li><strong>average</strong>: the average number of cercariae produced by each parasite genotype over the 4 weeks of shedding.</li> <li><strong>PO</strong>: the total phenoloxidase activity in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>2</sup>.</li> <li><strong>Hb</strong>: the hemoglobin rate in infected snail hemolymph, measured at 7.5 weeks post-exposure <sup>3</sup>.</li> </ul> <p> </p> <p><strong>sex.csv</strong></p> <p> </p> <p>This table contains the <em>in silico</em> sexing of F0 parents, F1 parents and F2 progeny of <em>S. mansoni</em> parasites.</p> <p>This table is made of 4 columns:</p> <ul> <li><strong>id</strong>: the unique identifier of each sample</li> <li><strong>read_depth</strong>: the read depth ratio between the Z-linked and pseudo-autosomal regions.</li> <li><strong>ratio</strong>: computed ratio between the Z-linked and pseudo-autosomal regions.</li> <li><strong>sex</strong>: the sex of each parasite genotype determined <em>in silico</em>: a ratio around 1 corresponds to a male carrying two Z chromosomes while a ratio around 0.5 corresponds to a female carrying only one Z chromosome.</li> </ul> <p><strong>Notes:</strong></p> <p><sup>1</sup>. Le Clec’h W, Chevalier F et al. Real-time PCR for sexing Schistosoma mansoni cercariae. Mol Biochem Parasitol. Jan-Feb 2016; 205(1-2):35-8.doi: 10.1016/j.molbiopara.2016.03.010. Epub 2016 Mar 26.</p> <p><sup>2</sup>. Le Clec’h W et al. Characterization of hemolymph phenoloxidase activity in two Biomphalaria snail species and impact of Schistosoma mansoni infection. Parasit Vectors. 2016 Jan 22; 9:32.doi: 10.1186/s13071-016-1319-6.</p> <p><sup>3</sup>. Le Clec'h et al. Striking differences in virulence, transmission and sporocyst growth dynamics between two schistosome populations. Parasit Vectors. 2019 Oct 16; 12(1):485. doi: 10.1186/s13071-019-3741-z.</p>
Fig. 4 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system
Fig. 4. Total number of a) genotype-I and b) genotype-II myxospores produced per actinospore, as a measure of parasite success, in fish from single and mixedgenotype treatments. Black bars denote genotype-I only, white denote genotype-II only, and grey denote mixed-genotype treatments. Letters indicate treatments that differed (Tukey's HSD tests, α = 0.05).
Fig. 3 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system
Fig. 3. Parasite copy number, as a measure of parasite competition in mixed-genotype treatments, in a) gill tissue sampled at 7d (t7), b) gill tissue sampled at 14d (t14) c) intestinal tissue sampled at 7d, and d) intestinal tissue sampled at 14d. Black bars denote genotype-I only, white denote genotype-II only, and grey denote mixedgenotype treatments. Inset striped grey bars represent total genotype I copy numbers, based on the proportion of genotype I in sequenced DNA samples (genotype II comprises the remainderthe solid grey bar). Letters indicate treatments that differed (Tukey's HSD tests, α = 0.05). Total number of genotype-I (black circles) and genotype-II (white circles) myxospores produced per actinospore, as a measure of parasite success in fish overlaid on parasite copy number in intestinal tissue sampled at 14d.
Fig. 2 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system
Fig. 2. Median day to death, as a measure of parasite virulence, in treatment groups. Black bars denote genotype-I only, white denote genotype-II only, and grey denote mixed-genotype treatments. Letters indicate treatments that differed (Tukey's HSD tests, α = 0.05).
Fig. 1 in Outcome of within-host competition demonstrates that parasite virulence doesn't equal success in a myxozoan model system
Fig. 1. Experimental schematic and timeline. Timeline begins at t-3 when density of parasites in polychaete cultures (inset a) was estimated in replicate water samples to calculate dose administered on t0 and t6. Specific-pathogen-free (SPF) well water ("W") was used as a negative control and a mock exposure t0 and t6 in treatments that received no parasites on those exposure dates "W"- denotes water, "I: denotes genotype-I and "II" denotes genotype-II (inset b). * denote treatments used for cytokine and immunoglobulin assays (b).
Out of the 'host' box: Extreme off-host conditions alter the infectivity and virulence of a parasitic bacterium
<p>Disease agents play an important role in the ecology and life history of wild and cultivated populations and communities. While most studies focus on the adaptation of parasites to their hosts, the adaptation of free-living parasite stages to their external (off-host) environment may tell us a lot about the factors that shape the distribution of parasites. <em>Pasteuria</em> <em>ramosa</em> is an endoparasitic bacterium of the water flea <em>Daphnia</em> with a wide geographic distribution. Its transmission stages rest outside of the host and thus experience varying environmental regimes. We examined the life history of <em>P</em>. <em>ramosa</em> populations from four environmental conditions (i.e., groups of habitats): the factorial combinations of summer-dry water bodies or not, and winter-freeze water bodies or not. Our goal was to examine how the combination of winter temperature and summer dryness affects the parasite's ability to attach to its host and to infect it. We subjected samples of the four groups of habitats to temperatures of 20, 33, 46 and 60˚C in dry and wet conditions, and exposed a susceptible clone of <em>Daphnia magna</em> to the treated spores. We found that spores that had undergone desiccation endured higher temperatures better than spores kept wet, both regarding attachment and subsequent infection. Furthermore, spores treated with heightened temperatures were much less infective and virulent. Even under high temperatures (60˚C), exposed spores from all populations were able to attach to the host cuticle, albeit they were unable to establish infection. Our work highlights the sensitivity of a host-free resting stage of a bacterial parasite to the external environment. Long heatwaves and harsh summers, which are becoming more frequent due to recent climate changes, may therefore pose a problem for parasite survival.</p>
High parasite virulence necessary for the maintenance of host outcrossing via parasite-mediated selection
<p>Biparental sex is widespread in nature, yet costly relative to uniparental reproduction. It is generally unclear why self-fertilizing or asexual lineages do not readily invade outcrossing populations. The Red Queen hypothesis predicts that coevolving parasites can prevent self-fertilizing or asexual lineages from invading outcrossing host populations. However, only highly virulent parasites are predicted to maintain outcrossing, which may limit the general applicability of the Red Queen hypothesis. Here, we tested whether the ability of coevolving parasites to prevent invasion of self-fertilization within outcrossing host populations was dependent on parasite virulence. We introduced wild-type <em>Caenorhabditis elegans</em> hermaphrodites, capable of both self-fertilization and outcrossing, into <em>C. elegans</em> populations fixed for a mutant allele conferring obligate outcrossing. Replicate <em>C. elegans</em> populations were exposed for 24 host generations to one of four strains of <em>Serratia marcescens</em> parasites that varied in virulence, under three treatments: a heat-killed (control, non-infectious) parasite treatment, a fixed-genotype (non-evolving) parasite treatment, and a copassaged (potentially coevolving) parasite treatment. As predicted, self-fertilization invaded <em>C. elegans</em> host populations in the control and fixed-parasite treatments, regardless of parasite virulence. In the copassaged treatment, selfing invaded host populations coevolving with low- to mid- virulent strains but remained rare in hosts coevolving with highly virulent bacterial strains. Therefore, we found that only highly virulent coevolving parasites can impede the invasion of selfing.</p>
High parasite virulence necessary for the maintenance of host outcrossing via parasite-mediated selection
Open the record for dataset details and reuse information.
Out of the ‘host’ box: Extreme off-host conditions alter the infectivity and virulence of a parasitic bacterium
Open the record for dataset details and reuse information.
Resource fluctuations inhibit the reproduction and virulence of the human parasite Schistosoma mansoni in its snail intermediate host
Resource availability can powerfully influence host-parasite interactions. However, we currently lack a mechanistic framework to predict how resource fluctuations alter individual infection dynamics. We address this gap with experiments manipulating resource supply and starvation for a human parasite, Schistosoma mansoni, and its snail intermediate host to test a hypothesis derived from mechanistic energy budget theory: resource fluctuations should reduce schistosome reproduction and virulence by inhibiting parasite ingestion of host biomass. Low resource supply caused hosts to remain small, reproduce less, and produce fewer human-infectious cercariae. Periodic starvation also inhibited cercarial production and prevented infection-induced castration. The periodic starvation experiment also revealed substantial differences in fit between two bioenergetic model variants, which differ in their representation of host starvation. Simulations using the best fit parameters of the winning model suggest that schistosome performance substantially declines with resource fluctuations with periods >7 days. These experiments strengthen mechanistic theory that can be readily scaled up to the population level to understand key feedbacks between resources, host population dynamics, parasitism, and control interventions. Integrating resources with other environmental drivers of disease in an explicit bioenergetic framework could ultimately yield mechanistic predictions for many disease systems.
Data from: Elevated atmospheric concentrations of carbon dioxide reduce monarch tolerance and increase parasite virulence by altering the medicinal properties of milkweeds
Hosts combat their parasites using mechanisms of resistance and tolerance, which together determine parasite virulence. Environmental factors, including diet, mediate the impact of parasites on hosts, with diet providing nutritional and medicinal properties. Here, we present the first evidence that ongoing environmental change decreases host tolerance and increases parasite virulence through a loss of dietary medicinal quality. Monarch butterflies use dietary toxins (cardenolides) to reduce the deleterious impacts of a protozoan parasite. We fed monarch larvae foliage from four milkweed species grown under either elevated or ambient CO2, and measured changes in resistance, tolerance, and virulence. The most high-cardenolide milkweed species lost its medicinal properties under elevated CO2; monarch tolerance to infection decreased, and parasite virulence increased. Declines in medicinal quality were associated with declines in foliar concentrations of lipophilic cardenolides. Our results emphasize that global environmental change may influence parasite-host interactions through changes in the medicinal properties of plants.
Soybean HPR virulence and parasitism by Aphelinus
Open the record for dataset details and reuse information.
Data from: Multiple transmission routes sustain high prevalence of a virulent parasite in a butterfly host
Open the record for dataset details and reuse information.
Data from: Elevated atmospheric concentrations of carbon dioxide reduce monarch tolerance and increase parasite virulence by altering the medicinal properties of milkweeds
Open the record for dataset details and reuse information.
Resource fluctuations inhibit the reproduction and virulence of the human parasite Schistosoma mansoni in its snail intermediate host
Open the record for dataset details and reuse information.
Coinfection accelerates transmission to new hosts despite no effects on virulence and parasite growth
Open the record for dataset details and reuse information.
Transcriptome-wide comparisons and virulence gene polymorphisms of host-associated genotypes of the cnidarian parasite Ceratonova shasta in salmonids
<p><i>Ceratonova shasta</i> is an important myxozoan pathogen affecting the health of salmonid fishes in the Pacific Northwest of North America. <i>C. shasta</i> exists as a complex of host-specific genotypes, some with low to moderate virulence, and one that causes a profound, lethal infection in susceptible hosts. High throughput sequencing methods are powerful tools for discovering the genetic basis of these host/virulence differences, but deep sequencing of myxozoans has been challenging due to extremely fast molecular evolution of this group, yielding strongly divergent sequences that are difficult to identify, and unavoidable host contamination. We designed and optimized different bioinformatic pipelines to address these challenges. We obtained a unique set of comprehensive, host-free myxozoan RNA-seq data from <i>C. shasta </i>genotypes of varying virulence from different salmonid hosts. Analyses of transcriptome-wide genetic distances and maximum likelihood multigene phylogenies elucidated the evolutionary relationship between lineages and demonstrated the limited resolution of the established Internal Transcribed Spacer marker for <i>C. shasta</i> genotype identification, as this marker fails to differentiate between biologically distinct genotype II lineages from coho salmon and rainbow trout. We further analyzed the datasets based on polymorphisms in two gene groups related to virulence: cell migration and proteolytic enzymes including their inhibitors. The developed SNP-calling pipeline identified polymorphisms between genotypes and demonstrated that variations in both motility and protease genes were associated with different levels of virulence of <i>C. shasta</i> in its salmonid hosts. The prospective use of proteolytic enzymes as promising candidates for targeted interventions against myxozoans in aquaculture is discussed. We developed host-free transcriptomes of a myxozoan model organism from strains that exhibited different degrees of virulence, as a unique source of data that will foster functional gene analyses and serve as a base for the development of potential therapeutics for efficient control of these parasites.</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: 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.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.