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520 results for “Host interactions”
The Pathogen-Host Interactions Database, version 4.18
<p>PHI-base is an online database (available at <a href="http://www.phi-base.org">phi-base.org</a>) that catalogues experimentally verified pathogenicity, virulence and effector genes from fungal, oomycete and bacterial pathogens, which infect animal, plant, fungal and insect hosts. PHI-base is a valuable resource in the discovery of genes in medically and agronomically important pathogens, which may be potential targets for chemical intervention.</p> <p>Each entry in PHI-base is curated by domain experts and is supported by strong experimental evidence (for example, gene disruption and gene complementation experiments), as well as literature references in which the original experiments are described. Each gene in PHI-base is presented with its nucleotide sequence and deduced amino acid sequence (available in a FASTA file), as well as a detailed description of the predicted protein's function during the host infection process. To facilitate data interoperability, we have annotated genes using ontologies, controlled vocabularies, and links to external sources (including UniProt, Gene Ontology, Enzyme Commission, NCBI Taxonomy, EMBL, PubMed and FRAC).</p> <p>This PHI-base dataset is a Frictionless Data Package that contains an export of the PHI-base database in CSV format (comma-separated values), plus a FASTA file with sequences for each gene in the database. This version of the dataset, version 4.18, contains 5,828 publications, covering 23,497 pathogen–host interactions and 10,614 pathogen genes across 335 pathogen species and 265 host species.</p>
Graphic Illustration of Kendra Phelp's Talk: A harmonized taxonomic resource is critical for accurately interpreting host-pathogen interactions
<p><a href="https://lib.ku.edu/people/courtney-foat" target="_blank" rel="noopener">Courtney Foat</a>, Advisor for Strategic Initiatives & Organizational Engagement at the University of Kansas, graphically recorded this invited talk by Kendra Phelps at an NSF-supported Workshop: Digital Collections Data and Tracking Disease.</p>
PHI-base: the Pathogen-Host Interactions Database, version 5.1
<p><strong>Download the dataset here: <a title="Download PHI-base 5.1" href="https://zenodo.org/records/16738930/files/phi-base_v5.1.zip?download=1">phi-base_v5.1.zip</a></strong></p> <p>The Pathogen–Host Interactions Database (PHI-base) is an online database that catalogues experimentally-verified pathogenicity, virulence and effector genes from fungal, oomycete, and bacterial pathogens, which infect animal, plant, fungal, and insect hosts. PHI-base is a valuable resource in the discovery of genes in medically and agronomically important pathogens, which may be potential targets for chemical intervention.</p> <p>Information in PHI-base is manually curated by domain experts and is supported by strong experimental evidence (for example, gene disruption and gene complementation experiments), as well as references to the literature in which the original experiments are described. Annotations are made using terms from ontologies and controlled vocabularies, including the <a href="https://www.geneontology.org/">Gene Ontology</a> (GO), <a href="https://pubmed.ncbi.nlm.nih.gov/21030441/">Brenda Tissue Ontology</a> (BTO), and the <a href="https://obofoundry.org/ontology/phipo.html">Pathogen–Host Interaction Phenotype Ontology</a> (PHIPO).</p> <p>PHI-base 5 includes data that was curated using a new curation process described in <a href="https://doi.org/10.7554/eLife.84658">Cuzick et. al</a> (2023). Data releases for PHI-base 5 do not use the same schema as data releases from PHI-base 4, but all data records from PHI-base 4 that can be made compatible with the new schema are included with this release. Data releases from PHI-base 4 and PHI-base 5 will occur in parallel until such time that all data from PHI-base 4 can be migrated to PHI-base 5. The PHI-base 4 data releases are available on Zenodo at <a href="https://zenodo.org/doi/10.5281/zenodo.5356870">https://zenodo.org/doi/10.5281/zenodo.5356870</a>.</p> <p>For more information about the planned transition from PHI-base 4 to PHI-base 5, see the <a href="https://phi5.phi-base.org/#/help">Help</a> and <a href="https://phi5.phi-base.org/#/announcements">Announcements</a> page on the PHI-base 5 website.</p> <h2>Release statistics</h2> <p>This version of the PHI-base 5 dataset contains the following types of information:</p> <table style="border-collapse: collapse; border-width: 1px; width: 40.2168%; height: 362.8px;"> <thead> <tr style="height: 19.6px;"> <th style="border-width: 1px; width: 84.846%; height: 19.6px;">Data type</th> <th style="border-width: 1px; width: 15.4054%; height: 19.6px;">Count</th> </tr> </thead> <tbody> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Genes</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">9457</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Interactions</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">31094</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Pathogen species</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">303</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Host species</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">237</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Diseases</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">343</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">References</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">5202</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;"><strong>Annotations</strong></td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;"> </td> </tr> <tr style="height: 10px;"> <td style="border-width: 1px; width: 84.846%; height: 10px;">Pathogen-host interaction phenotype</td> <td style="border-width: 1px; width: 15.4054%; height: 10px;">18260</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Gene-for-gene phenotype</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">452</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Pathogen phenotype</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">9413</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Host phenotype</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">14</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">GO biological process</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">1453</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">GO cellular component</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">85</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">GO molecular function</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">152</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Post-translational modification</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">6</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">Physical interaction</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">53</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">WT RNA expression</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">36</td> </tr> <tr style="height: 19.6px;"> <td style="border-width: 1px; width: 84.846%; height: 19.6px;">WT protein expression</td> <td style="border-width: 1px; width: 15.4054%; height: 19.6px;">2</td> </tr> </tbody> </table> <h2>File contents</h2> <ul> <li> <p><strong>phi-base_v5.1.xlsx</strong>: the PHI-base dataset as an Excel spreadsheet. This format follows the layout of the PHI-base 5 website, with sheets corresponding to the sections of gene pages on the website. This format is designed for use by non-technical users.</p> </li> <li> <p><strong>phi-base_v5.1.json</strong>: the PHI-base dataset in JSON format. This is modelled on the export format used by PHI-Canto, the curation tool used by PHI-base. This format is primarily intended for programmatic usage and has additional information (e.g. metadata for curation sessions) that is not included in the spreadsheet format.</p> </li> <li> <p><strong>phi-base.schema.json</strong>: a <a href="https://json-schema.org/">JSON Schema</a> file for the JSON format of the dataset. This is included as documentation for the fields in the JSON file, but can also be used to validate the dataset.</p> </li> </ul>
PhasAGE Training School 1 - Phase separation in virus-host interactions- LECTURE
<p>The Training School 1 <strong>“Computational Methods to Study Protein Phase Separation”</strong> is the first edition of a series of PhasAGE training activities.</p> <p>The goal of this course is to provide participants with the basic knowledge to understand the phenomenon of <strong>Phase Separation</strong>, its role in biological processes and diseases. In addition, the course will provide <strong>an overview of the available computational resources</strong> to navigate this knowledge. Participants will have <strong>hands-on training</strong> in tools and resources available for life sciences, to collect information from the literature on biomolecular phase transitions, identify features triggering phase transitions, mutations associated with diseases, known or predicted PTMs and molecular interaction sites.</p>
Geographic range size and species morphology determines the organization of sponge host-guest interaction networks across tropical coral reefs (Raw data)
<p>Datasets for the analysis developed in the Article "<em><strong>Geographic range size and species morphology determines the organization of sponge host-guest interaction networks across tropical coral reefs</strong></em>". For more information, please refer to the original publication.</p> <p>Network_Structural_Index_&_SpogeTraits.csv <- Structural Index for the sponge-dwelling fauna network, sponge accumulated area and sponges’ morphology.</p> <p>NWTA_CoralReefs_Sponges_ interactions.csv <- Relationship between host sponges and guest fauna in the Northwester Atlantic coral reefs</p> <p>NWTA_CoralReefs_Sponge_reacords.csv <- Sponge species incidence records in the Northwester Atlantic coral reefs</p> <p>sponges_morphological_description.csv <- Sponge morphological standardization</p> <p>Network.html <- Interactive sponge-dwelling fauna network</p> <p>Enjoy!<br> </p>
Data from: Deciphering host-parasitoid interactions and parasitism rates of crop pests using DNA metabarcoding
Open the record for dataset details and reuse information.
Decoding host-microbiome interactions through co-expression network analysis within the non-human primate intestine
<p>Supplementary Table Captions:</p> <p>Supplementary Table S9. Evaluation and parameter determination of host and microbiome RNA read classification using simulation datasets</p> <p>Supplementary Table S10. 40 pathways significantly upregulated in the cecum as compared to the transverse colon</p> <p>Supplementary Table S11. Host-microbiome gene co-expression network edges</p> <p>Supplementary Table S12. Host-host gene co-expression network edges</p> <p>Supplementary Table S13. Microbiome-microbiome gene co-expression network edges</p> <p>Supplementary Table S14. List of genes included in each gene module identified from the gene co-expression network</p> <p>Supplementary Table S15. Results of enrichment analysis for each gene module identified from the gene co-expression network</p> <p>Supplementary Table S16. The top 32 bacterial species in terms of expression abundance based on metatranscriptome profiles</p> <p>Supplementary Table S17. Number of microbiome RNA reads annotated by the KEGG database</p> <p>Supplementary Table S18. Results of enrichment analysis of gene modules for each parameter</p> <p>Supplementary Table S19. Evaluation of modules in each parameter of Newman algorithm</p> <p>Supplementary Table S20. Evaluation of modules in each parameter of Louvain algorithm</p> <p>Supplementary Table S21. Evaluation of modules in each parameter of Leiden algorithm</p> <p>Supplementary Table S22. Evaluation of modules in each parameter of WGCNA</p>
Data from: Extreme heat reduces host and parasite performance in a butterfly-parasite interaction
<p>Environmental temperature fundamentally shapes insect physiology, fitness, and interactions with parasites. Differential climate warming effects on host versus parasite biology could exacerbate or inhibit parasite transmission, with far-reaching implications for pollination services, biocontrol, and human health. Here, we experimentally test how controlled temperatures influence multiple components of host and parasite fitness in monarch butterflies (<em>Danaus plexippus</em>) and their protozoan parasites <em>Ophryocystis elektroscirrha</em>. Using five constant temperature treatments spanning 18-34°C, we measured monarch development, survival, size, immune function, and parasite infection status and intensity. Monarch size and survival declined sharply at 34°C, as did infection probability, suggesting that hot temperatures decrease both host and parasite performance. The lack of infection at 34°C was not due to greater host immunity or faster larval development but could instead reflect the thermal limits of parasite invasion and within-host replication. In the context of ongoing climate change, our experiment suggests that temperature increases above the upper thermal range will reduce the fitness of both monarchs and their parasites, with lower infection rates potentially mitigating the impact of extreme heat on future monarch abundance and distribution.</p>
Data from: The interactive effects of heat stress, parasitism, and hostplant quality in a host-parasitoid system
<p>Species interactions are expected to change in myriad ways as the frequency and magnitude of extreme temperature events increase with anthropogenic climate change. The relationships between endosymbionts, parasites, and their hosts are particularly sensitive to thermal stress, which can have cascading effects to other trophic levels. We investigate the interactive effects of heat stress and parasitism on a terrestrial tritrophic system consisting of two hostplants (one common, high-quality plant and one novel, low-quality plant), a caterpillar herbivore, and a specialist parasitoid wasp. We used a fully-factorial experiment to determine the bottom-up effects of the novel hostplant on both the caterpillars' life history traits and the wasps' survival, and the top-down effects of parasitism and heat shock on caterpillar developmental outcomes and herbivory levels. Hostplant identity interacted with thermal stress to affect wasp success, with wasps performing better on the low-quality hostplant under constant temperatures but worse under heat shock conditions. Surprisingly, caterpillars consumed less leaf material of the low-quality hostplant to reach the same final mass across developmental outcomes. In parasitized caterpillars, heat shock reduced parasitoid survival and increased both caterpillar final mass and development time on both hostplants. These findings highlight the importance of studying community-level responses to climate change from a holistic and integrative perspective and provide insight into potential substantial interactions between thermal stress and diet quality in plant-insect systems.</p>
The impact of within-host coinfection interactions on between-host parasite transmission dynamics varies with spatial scale
<p>Within-host interactions among coinfecting parasites can have major consequences for individual infection risk and disease severity. However, the impact of these within-host interactions on between-host parasite transmission, and the spatial scales over which they occur, remain unknown. We developed and applied a novel spatially explicit analysis to parasite infection data from a wild wood mouse (<em>Apodemus sylvaticus</em>) population. We previously demonstrated a strong within-host negative interaction between two wood mouse gastrointestinal parasites, the nematode <em>Heligmosomoides polygyrus,</em> and the coccidian <em>Eimeria hungaryensis</em>, using drug-treatment experiments. Here, we show this negative within-host interaction can significantly alter the between-host transmission dynamics of <em>E. hungaryensis</em>, but only within spatially-restricted neighbourhoods around each host. However, for the closely related species <em>E. apionodes</em>, which experiments show does not interact strongly with <em>H. polygyrus</em>, we did not find any effect on transmission over any spatial scale. Our results demonstrate that the effects of within-host coinfection interactions can ripple out beyond each host to alter the transmission dynamics of the parasites, but only over local scales that likely reflect the spatial dimension of transmission. Hence there may be knock-on consequences of drug treatments impacting the transmission of non-target parasites, altering infection risks even for non-treated individuals in the wider neighbourhood.</p>
Complex plant quality - microbiota - population interactions modulate the response of a specialist herbivore to the defense of its host plant.
<p>1. Many specialist herbivores have evolved strategies to cope with plant defenses, with gut microbiota potentially participating to such adaptations.</p> <p>2. In this study we assessed whether the history of plant use (population origin) and microbiota may interact with plant defense adaptation.</p> <p>3. We tested whether microbiota enhance the performance of <em>Melitaea cinxia </em>larvae on their host plant, <em>Plantago lanceolata</em> and increase their ability to cope the defensive compounds, iridoid glycosides (IGs).</p> <p>3. The gut microbiota was significantly affected by both larval population origin and host plant IG level. Contrary to our prediction, impoverishing the microbiota with antibiotic treatment did not reduce larval performance.</p> <p>5. As expected for this specialized insect herbivore, sequestration of one of IGs was higher in larvae fed with plants producing higher concentration of IGs. These larvae also showed metabolic signature of intoxication (<em>i.e. </em>decrease in Lysine levels). However, intoxication on highly defended plants was only observed when larvae with history of poorly defended plants were simultaneously treated with antibiotics.</p> <p>6. Our results suggest that both adaptation and microbiota contribute to the metabolic response of herbivores to plant defense though complex interactions.</p>
A model of within-host interactions between host resources, macroparasite infection and immune response
<p>This project was designed to mathematically investigate the of different host parasite-mitigation strategies on host condition. The R code herein comprises:</p> <ul> <li>An ODE model of within-host interactions between a macroparasite (e.g. helminth) infection, host resource levels and host immune response, and the consequent effects on host condition. In brief, resources are ingested and utilised by the host, leading to inceased condition. The host is infected by a parasite, which matures and establishes within the host; both age stages cause harm to the host, decreasing host condition. The presence of the parasite stimulates an immune response, which can either target larval or adult parasites (a resistance strategy), or ameliorate the harm they cause (a tolerance strategy). The host can also reduce resource intake in order to also reduce ingestion of parasite infective stages (an avoidance strategy). Resistance responses have an associated immunopathology, in that the immune response also harms the host.</li> <li>Code to plot model trajectories over time.</li> <li>Code to plot multiple trajectories as a heat map, in which the x-axis is time and the y-axis is a parameter representing the host investment in its parasite-mitigation strategy.</li> <li>Code to calculate the optimum host investment for each strategy, over various sets of parameter values, as determined by maximising mean host condition over a given timeframe, and to plot the output.</li> <li>The same are also provided for an ODE model in which the total immune response is allocated between the two resistance responses and tolerance (a combined strategy). The optimisation code optimises both the total investment in immune repsonse, and how much is allocated to the three different individual strategies.</li> </ul> <p>The model and results are described in detail in the associated manuscript. We also provide here the simulated datasets in which the optimum host investments were calculated over a range of different parameter values, as these take several hours to run on a standard desktop computer..</p>
Profiling phage-host interactions between Skunavirus receptor binding proteins and lactococcal cell wall polysaccharide structures
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Fig. 10 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts
Fig. 10. Comparisons of inflammatory cells recruited to inflammatory foci in cane toads, Rhinella marina (a) and native frogs, Cyclorana australis (b). Each anuran species was exposed to infective larvae of Rhabdias hylae (white bars) and Rhabdias pseudosphaerocephala (grey bars). Graphs show average values ± 1 S.E.M.
Fig. 7 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts
Fig. 7. Histological investigation of lungworm infection in anurans. Graphs show the proportion of (a) metamorph native frogs (Cyclorana australis) and (b) metamorph cane toads (Rhinella marina) infected with lungworms, not infected with lungworms, or with inflammatory 'foci' (probable cases of a lungworm larva penetrating the anuran's body but failing to survive).
Fig. 2 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts
Fig. 2. The distribution of lungworm larvae in cane toad metamorphs. (a) Toad metamorphs infected with Rhabdias hylae (native frog lungworm) and (b) toad metamorphs infected with Rhabdias pseudosphaerocephala (cane toad lungworm). Data in panel (b) are from Pizzatto et al. (2010), with permission. LUNG refers to adult lungworms found within the lung, SKIN/MUSCLE refers to larvae found in the skeletal muscle or subcutaneous tissue, HEAD refers to larvae detected in the head or neck region (excluding those found in eye tissue), EYE indicates larvae found in the eye or periocular tissue, and COELOM denotes larvae within the coelom or coelomic membranes.
Fig. 1. Histological image depicting a in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts
Fig. 1. Histological image depicting a transverse section of (a) R. hylae larva in the connective tissue of the head of a cane toad and (b) the inflammatory response composed primarily of macrophages and multinucleated giant cells surrounding the parasite. Haematoxylin and eosin stain, 400× magnification, scale bar equals 30 μm.
Fig. 4 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts
Fig. 4. Effect of time since exposure to Rhabdias hylae larvae on cane toad metamorphs: (a) shows the number of larvae found in toads and (b) shows the number of foci (areas of inflammation with no visible larvae) in toads, as determined by histological methods.
Fig. 9 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts
Fig. 9. Change in the average number of inflammatory foci (probable cases of larval parasites breaking down) observed in all anurans over time. Graph shows average values ± 1 S.E.M.
Fig. 6 in Host-parasite interactions during a biological invasion: The fate of lungworms (Rhabdias spp.) inside native and novel anuran hosts
Fig. 6. Effects of Rhabdias hylae infection on cane toad metamorphs: (a) the average percentage of neutrophils and (b) lymphocytes around inflammation sites over time in cane toads infected with Rhabdias hylae. Graphs show average values ±1 S.E.M.
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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.