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886 results for “immune infection”
Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection
<p><strong>scRNA-seq data</strong></p> <p>Data were processed using cellranger v 4.0.0 with the refdata-gex-GRCh38-2020-A reference.</p> <p><em>h5files.zip</em>: contains all h5-Files of raw feature-barcode counts (e.g. 20094_0001_A_B_raw_feature_bc_matrix.new.h5 )</p> <p><em>raw_feature_bc_matrices.zip</em>: contains the <em>same data</em> as h5files.zip, but also in mtx-format.</p> <p>covid_object_ncomms<em>.RDS</em>: contains the Seurat file with which all analyses were conducted.</p> <p><em>samples2condition.df</em>: text file containing sample to condition information</p> <p><strong>Bulk RNA-seq</strong></p> <p><em>covid_bulk.zip</em> contains the count matrices extracted from the zUMIs runs for the bulk cohort.</p> <p><em>nasal_swabs.zip</em> contains the count matrices extracted from the zUMIs run for the nasal swab cohort.</p> <p>The extracted count matrices were then used with the bulk analysis scripts provided with the source code.</p> <p><strong>Source Code</strong></p> <p>All <strong>source code</strong> for the publication is available from: <a href="https://github.com/mjoppich/covidSC">https://github.com/mjoppich/covidSC</a> or from tagged releases: <a href="https://github.com/mjoppich/covidSC/releases/tag/ncomms">https://github.com/mjoppich/covidSC/releases/tag/ncomms</a></p> <p>When using any of these data, please cite:<br> <br> Pekayvaz et al., Protective immune trajectories in early viral containment of non-pneumonic SARS-CoV-2 infection, Nature Communications 2022</p>
Raw data for the article: Successful Use of Heterologous CMV-Reactive T Lymphocyte to Treat Severe Refractory Cytomegalovirus (CMV) Infection in a Liver Transplanted Patient: Correlation of the Host Antiviral Immune Reconstitution with CMV Viral Load and CMV miRNome
<p>Cytomegalovirus (CMV) infection is the most significant viral infection in hosts with compromised immune systems as solid organ transplant patients. Despite significant progress being made in the prevention of CMV disease in these patients, further therapeutic strategies for CMV disease and for the CMV reactivation prevention are needed. Here, we describe the outcome of the infusion of in vitro expanded CMV-reactive T-cells, taken from a healthy CMV-seropositive donor, in a liver-transplanted recipient with a refractory recurrent CMV. In this particular case, adoptive transfer of allogenic CMV-reactive T-lymphocytes resulted in the clearance of CMV infection and resolution of the pathological manifestations of the patient. In the study we also investigated circulating miRNAs, both cellular and viral, as potential biomarkers during the course of CMV infection. The results indicate that the infusion of allogenic CMV-reactive T-cells can be an effective strategy to treat CMV infection recurrence when the generation of autologous virus specific T cell clones is not possible.</p>
Neutralizing immunity induced against the Omicron BA.2 variant in vaccinated and unvaccinated individuals infected by Omicron BA.1
<p>This repository contains the pertinent data files used in the manuscript, <em>Neutralizing immunity induced against the Omicron BA.2 variant in vaccinated and unvaccinated individuals infected by Omicron BA.1</em>.</p>
Dataset for the manuscript: Modelling the within-host spread of SARS-CoV-2 infection, and the subsequent immune response, using a hybrid, multiscale, individual-based model. Part I: Macrophages.
<p>Dataset for the manuscript:</p> <p>Modelling the within-host spread of SARS-CoV-2 infection, and the subsequent immune response, using a hybrid, multiscale, individual-based model. Part I: Macrophages. preprint, bioRxiv, 2022. DOI: 10.1101/2022.05.06.490883</p> <p>Each zip file contains the raw computational data (as a gzip compressed tarball), YAML input files, as well as Python plotting scripts. The Python plotting scripts have dependencies on the packages: <em>tarfile</em>, <em>multiprocessing</em>, <em>numpy</em>, <em>scipy</em>, and <em>matplotlib</em>. Note that the Python plotting scripts plot directly from the gzip compressed tarballs.</p> <p>The corresponding code can be found on GitHub: https://github.com/Ruth-Bowness-Group/CAModel</p>
Helminth-associated changes in host immune phenotype connect top-down and bottom-up interactions during co-infection
<p>Within-host parasite interactions can be mediated by the host and changes in host phenotypes often serve as indicators of the presence or intensity of parasite interactions.</p> <p>Parasites like helminths induce a range of physiological, morphological, and immunological changes in hosts that can drive bottom-up (resource-mediated) or top-down (immune-mediated) interactions with co-infecting parasites. Although top-down and bottom-up interactions are typically studied in isolation, the diverse phenotypic changes induced by parasite infection may serve as a useful tool for understanding if, and when, these processes act in concert.</p> <p>Using an anthelmintic treatment study of African buffalo (Syncerus caffer), we tracked changes in host immunological and morphological phenotypes during helminth-coccidia co-infection to investigate their role in driving independent and combinatorial bottom-up and top-down parasite interactions. We also examined repercussions for host fitness.</p> <p>Clearance of a blood-sucking helminth, Haemonchus, from the host gastrointestinal tract induced a systemic Th2 immune phenotype, while clearance of a tissue-feeding helminth, Cooperia, induced a systemic Th1 phenotype. Furthermore, the Haemonchus-associated systemic Th2 immune phenotype drove simultaneous top-down and bottom-up effects that increased coccidia shedding by changing the immunological and morphological landscapes of the intestine.</p> <p>Higher coccidia shedding was associated with lower host body condition, a lower chance of pregnancy, and older age at first pregnancy, suggesting that coccidia infection imposed significant condition and reproductive costs on the host.</p> <p>Our findings suggest that top-down and bottom-up interactions may commonly co-occur and that tracking key host phenotypes that change in response to infection can help uncover complex pathways by which parasites interact.</p>
Raw Data for the article: Analysis of the Specific Immune Response after the Third Dose of mRNA COVID-19 Vaccines in Organ Transplant Recipients: Possible Spike-S1 Reactive IgA Signature in Protection from SARS-CoV-2 Infection
<p><strong>Background:</strong> Several studies have indicated that anti-SARS-CoV-2 mRNA vaccinations are less effective in inducing robust immune responses among solid organ transplant recipients (SOTRs) compared with the immunocompetent. The third dose of vaccine in SOTRs showed promising results of immunogenicity, even though clinical studies have suggested that immunocompromised subjects are less likely to build a protective immune response against SARS-CoV-2 resulting in lower vaccine efficacy for the prevention of severe COVID-19. <strong>Methods:</strong> Serological IgG and IgA were analyzed through CLIA or ELISA, respectively, while Spike-specific T cells were detected by ELISpot assay after the second and third dose of vaccine in 43 SOTRs. <strong>Results:</strong> The third dose induced an improvement in antibody response against SARS-CoV-2. We also reported a strong correlation between specific humoral and cellular responses after the third dose, even though we did not see significant changes in the magnitude of the SARS-CoV-2-specific T cell response. SOTRs who contracted the SARS-CoV-2 infection after the third dose, despite eliciting a positive IgG response, failed to mount an anti-Spike-S1 IgA response, both after the third dose and after SARS-CoV-2 infection. <strong>Conclusions:</strong> We can conclude that serum IgA detection can be helpful, along with IgG detection, for the evaluation of vaccine efficacy, principally in fragile subjects at high risk of infection.</p>
Ontogeny of immunity and potential implications for co-infection
<p>Immunity changes through ontogeny and can mediate facilitative and inhibitory interactions among co-infecting parasite species. In amphibians, most immune memory is not carried through metamorphosis, leading to variation in the complexity of immune responses across life stages. To test if the ontogeny of host immunity might drive interactions among co-infecting parasites, we simultaneously exposed Cuban treefrogs (<em>Osteopilus septentrionalis</em>) to a fungus (<em>Bactrachochytrium dendrobaditis</em>) and a nematode (<em>Aplectana hamatospicula</em>) at tadpole, metamorphic, and post-metamorphic life stages. We measured metrics of host immunity, host health, and parasite abundance. We predicted facilitative interactions between co-infecting parasites as the different immune responses hosts mount to combat these infectious are energetically challenging to mount simultaneously. We found ontogenetic differences in IgY levels and cellular immunity but no evidence that metamorphic frogs were more immunosuppressed than tadpoles. There was also little evidence that these parasites facilitated one another and no evidence that <em>A. hamatospicula </em>infection altered host immunity or health. However, Bd, which is known to be immunosuppressive, decreased immunity in metamorphic frogs. This made metamorphic frogs both less resistant and less tolerant of Bd infection than the other life stages. These findings indicate that changes in immunity altered host responses to parasite exposures throughout ontogeny.</p>
The genetics of immune and infection phenotypes in wild mice, Mus musculus domesticus
<p><span>Wild animals are under constant threat from a wide range of micro- and macroparasites in their environment. Animals make immune responses against parasites, and these are important in affecting the dynamics of parasite populations. Individual animals vary in their anti-parasite immune responses. Genetic polymorphism of immune-related loci contributes to inter-individual differences in immune responses, but most of what we know in this regard comes from studies of humans or laboratory animals; there are very few such studies of wild animals naturally infected with parasites. Here we have investigated the effect of Single Nucleotide Polymorphisms (SNPs) in immune-related loci (the MHC, and loci coding for cytokines and Toll-like receptors) on a wide range of immune and infection phenotypes in UK wild house mice, <em>Mus musculus domesticus</em>. We found strong associations between SNPs in various MHC and cytokine-coding loci on both immune measures (antibody concentration and cytokine production) and on infection phenotypes (infection with mites, worms and viruses). Our study provides a comprehensive view of how polymorphism of immune-related loci affects immune and infection phenotypes in naturally infected wild rodent populations.</span></p>
Safety, effectiveness, and skin immune response in a controlled human infection model of sand fly transmitted cutaneous leishmaniasis.
<p>Safety, effectiveness, and skin immune response in a controlled human infection model of sand fly transmitted cutaneous leishmaniasis.</p><p>Vivak Parkash1, Helen Ashwin1, Shoumit Dey1, Jovana Sadlova2, Barbora Vojtkova2, Katrien Van Bocxlaer1,3, Rebecca Wiggins1, David Thompson4 Nidhi Sharma Dey1, Charles L. Jaffe5, Eli Schwartz6, Petr Volf2, Charles J. N. Lacey1, Alison M. Layton1,3 * and Paul M. Kaye1,3 *.</p><p> </p><p>1 York Biomedical Research Institute, Hull York Medical School, University of York, York, UK</p><p>2 Department of Parasitology, Faculty of Science, Charles University, Viničná 7, Prague, Czech Republic</p><p>3 Skin Research Centre, Hull York Medical School, York, UK</p><p>4 York and Scarborough Teaching Hospitals NHS Foundation Trust, York, UK </p><p>5 Department of Microbiology and Molecular Genetics, Kuvin Center for the Study of Infectious and Tropical Diseases, IMRIC, The Hebrew University – Hadassah Medical School, Jerusalem, Israel</p><p>6 The Center for Geographic Medicine and Tropical Diseases, Chaim Sheba Medical Center, and The School of Medicine, Tel Aviv University, Israel.</p><p> </p><p>*Corresponding authors: paul.kaye@york.ac.uk and alison.layton@hyms.ac.uk</p><p> </p>
Safety of and Immune Response to Dolutegravir in HIV-1 Infected Infants, Children, and Adolescents
ClinicalTrials.gov study NCT01302847. IPD Sharing: Not stated. Countries: 8. Publications: 6.
Efficacy of Immunization With 4C-MenB in Preventing Experimental Urethral Infection With Neisseria Gonorrhoeae
ClinicalTrials.gov study NCT05294588. IPD Sharing: YES. Countries: 1. Publications: 1.
Safety and Immune Response to Vicriviroc in Combination Regimens in HIV-Infected ART Experienced Children and Adolescents
ClinicalTrials.gov study NCT00766597. IPD Sharing: Not stated. Countries: 2. Publications: 2.
Entecavir/Pegylated Interferon in Immune Tolerant Children With Chronic Hepatitis B Virus (HBV) Infection
ClinicalTrials.gov study NCT01368497. IPD Sharing: YES. Countries: 2. Publications: 1.
A Research Study to See if a Change in Therapy for HIV Infection Can Improve the Immune Response to Treatment
ClinicalTrials.gov study NCT00145795. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Study of SARS CoV-2 Infection and Potential Transmission in Individuals Immunized With Moderna COVID-19 Vaccine
ClinicalTrials.gov study NCT04811664. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Safety of and Immune Response to the Human Papillomavirus (HPV) Vaccine in HIV-Infected Women
ClinicalTrials.gov study NCT00604175. IPD Sharing: Not stated. Countries: 4. Publications: 8.
Safety of and Immune Response to a Meningitis Vaccine in HIV-Infected Children and Youth
ClinicalTrials.gov study NCT00459316. IPD Sharing: Not stated. Countries: 2. Publications: 10.
The Natural History of Severe Viral Infections and Characterization of Immune Defects in Patients Without Known Immunocompromise
ClinicalTrials.gov study NCT01011712. IPD Sharing: YES. Countries: 1. Publications: 3.
Immune Response and General Immune Health in Subjects Infected With Herpes Simplex Virus Type 1 (HSV-1)
ClinicalTrials.gov study NCT03661541. IPD Sharing: NO. Countries: 1. Publications: 1.
Study to Optimize the Quality of Samples for Cell-mediated Immunity (CMI) in ART-naïve HIV-1-infected Subjects
ClinicalTrials.gov study NCT01610427. IPD Sharing: NO. Countries: 1. Publications: 1.
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OpenNeuro
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