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727 results for “Viral infections”
Murine norovirus virulence factor 1 (VF1) protein contributes to viral fitness during persistent infection [Primary data]
<p>Primary data underlying journal article titled "<strong>Murine norovirus virulence factor 1 (VF1) protein contributes to viral fitness during persistent infection</strong>"</p>
Type III interferons may suppress viral infections by triggering cell death -- Imaging Dataset
<p>This dataset accompanies the article "Type III interferons may suppress viral infections by triggering cell death". Earlier version is available as a preprint, <a href="https://doi.org/10.1101/2024.09.09.612051" target="_blank" rel="noopener">https://doi.org/10.1101/2024.09.09.612051</a>. The updated dataset includes quantifications for Figure 7C and Figure 7D.</p>
Antagonism between viral infection and innate immunity at the single-cell level -- Immunostaining Imaging Dataset
<p>This dataset accompanies the article "Antagonism between viral infection and innate immunity at the single-cell level", at the time of submission available as a <a href="https://doi.org/10.1101/2022.11.18.517110">preprint</a>.</p>
Host-derived viral transporter protein for nitrogen uptake in infected marine phytoplankton
<p>Dataset for the article "Host-derived viral transporter protein for nitrogen uptake in infected marine phytoplankton", Monier et al.</p> <p>Data for all phylogenetic tree reconstructions (raw and masked protein sequence alignments in fasta format, tree file in newick format) and placement file (jplace format) of two environmental sequences are available.</p> <p>Data for all assay experiments are available: ammonium and urea assays, Omnilog phenotype screening (Nitrogen substrates).</p>
Deep-sequencing of viral genomes from treatment-naive HIV-infected persons shows positive association between intrahost genetic diversity and viral load
<p><strong><span>Background:</span></strong><span> Infection with human immunodeficiency virus type 1 (HIV) typically results from transmission of a small and genetically uniform viral population. Following transmission, the virus population becomes more diverse because of recombination and acquired mutations through genetic drift and selection. Viral intrahost genetic diversity remains a major obstacle to the cure of HIV; however, there is a disagreement whether intrahost viral genetic diversification associates positively or negatively with disease progression and progression markers. Viral load is a key progression marker and understanding its relationship to viral intrahost genetic diversity could help design future strategies for HIV monitoring and treatment.</span></p> <p><span><strong>Methods:</strong> </span><span>We analyzed deep-sequenced viral genomes from 2,650 treatment-naive HIV-infected persons to measure the intrahost genetic diversity of 2,447 genomic codon positions as calculated by Shannon entropy. We tested for associations between viral load (VL) and amino acid (AA) entropy accounting for sex, age, race, duration of infection, and HIV population structure.</span></p> <p><strong><span>Results:</span></strong><span><strong> </strong>We confirmed that the intrahost genetic diversity is highest in the <em>env</em> gene. Furthermore, we showed that mean Shannon entropy is significantly associated with VL, especially in infections of >24 months duration. We identified 16 significant associations between VL (p-value<2.0x10<sup>-5</sup>) and Shannon entropy at AA positions which in our association analysis explained 13% of the variance in VL.</span></p> <p><strong><span>Conclusions: </span></strong><span>Our results elucidate that viral intrahost genetic diversity is associated with VL and could be used as a better disease progression marker than HIV consensus sequence variants, especially in infections of longer duration. We emphasize that viral intrahost diversity should be considered when studying viral genomes and infection outcomes.</span></p>
Figure 2 in Peptidoglycan from Immunobiotic Lactobacillus rhamnosus Improves Resistance of Infant Mice to Respiratory Syncytial Viral Infection and Secondary Pneumococcal Pneumonia
Figure 2. – Photography of a juvenile lemon shark identified as Negaprion acutidens with an estimated total length of 70 cm (Photo MI).
Figure 1 in Peptidoglycan from Immunobiotic Lactobacillus rhamnosus Improves Resistance of Infant Mice to Respiratory Syncytial Viral Infection and Secondary Pneumococcal Pneumonia
Figure 1. – The Chesterfield islands (A) lie in the Coral Sea with New Caledonia (NC) to the east and Australia (AUS) to the west. The atoll structure of the Chesterfield (B) includes a V shaped barrier reef in the South (C) where the juvenile lemon sharks were observed (arrow).
HIV-1 control in vivo is related to the number but not the fraction of infected cells with viral unspliced RNA
<p>In the absence of antiretroviral therapy (ART), a subset of individuals, termed HIV controllers, have levels of plasma viremia that are orders of magnitude lower than non-controllers who are at higher risk for HIV disease progression. In addition to having fewer infected cells resulting in fewer cells with HIV RNA, it is possible that lower levels of plasma viremia in controllers is due to a lower fraction of the infected cells having HIV-1 unspliced RNA (HIV usRNA) compared with non-controllers. To directly test this possibility, we used sensitive and quantitative single cell sequencing methods to compare the fraction of infected cells that contain one or more copies of HIV usRNA in peripheral blood mononuclear cells (PBMC) obtained from controllers and non-controllers. The fraction of infected cells containing HIV usRNA did not differ between the two groups. Rather, the levels of viremia were strongly associated with the total number of infected cells that had HIV usRNA, as reported by others, with controllers having 34-fold fewer infected cells per million PBMC. These results reveal for the first time that viremic control is not associated with a lower fraction of proviruses expressing HIV usRNA, unlike what is reported for elite controllers, but is only related to having fewer infected cells overall, maybe reflecting greater immune clearance of infected cells. Our findings show that proviral silencing is not a key mechanism for viremic control and will help to refine strategies towards achieving HIV remission without ART.</p>
The central nervous system's proteogenomic and spatial imprint upon systemic viral infection, like SARS-CoV-2
<p>Data set including image files of histological stainings, immunohistochemistry, MELC, and spatial transcriptomics associated with the study mentioned above.</p>
IFN-γ primes bone marrow neutrophils to acquire regulatory functions in severe viral respiratory infections
Open the record for dataset details and reuse information.
Deep-sequencing of viral genomes from treatment-naive HIV-infected persons shows positive association between intrahost genetic diversity and viral load
Open the record for dataset details and reuse information.
TCRb repertoires of murine CD8T cells following viral infection
<p>TCRbeta repertoires from Tcf7-GFP transgenic GFP mice were FACS isolated and sequenced following viral infection. </p>
Raw data to: "Vectored antibody gene delivery restores host B and T cell control of persistent viral infection"
<p>Raw data underlying the publication by Ertuna et al. entitled "Vectored antibody gene delivery restores host B and T cell control of persistent viral infection"</p>
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>
Single-cell transcriptome analysis of the in vivo response to viral infection in the cave nectar bat Eonycteris spelaea
<p>Bats are reservoir hosts of many zoonotic viruses with pandemic potential in humans. Here, we<br> utilized single-cell transcriptome sequencing (scRNA-seq) to provide detailed comparative<br> analyses of the immune repertoire and the transcriptional responses in the bat lungs upon in<br> vivo infection with a double-stranded RNA virus, Pteropine orthoreovirus PRV3M. Neutrophils<br> were observed to have basally high IDO1 expression, uniquely amongst mammals currently<br> profiled by scRNA-seq. NK/T cells were the most abundant immune cell type in lung tissue, and<br> included three distinct CD8 + effector T cell populations delineated by the differential expression<br> of KLRB1, GFRA2 and DPP4. We identified NK/T clusters which up-regulated genes involved in<br> T-cell activation and effector function early after viral infection. Alveolar macrophages and<br> classical monocytes were key drivers of antiviral interferon signaling. Infection also resulted in<br> the expansion of a CSF1R + population expressing collagen-like genes, which became the<br> predominant myeloid cell type after infection. This work uncovers novel features relevant to viral<br> disease tolerance in bats, lays a foundation for future in vivo and in vitro experimental<br> investigations, and serves as a key resource for comparative immunology studies across bats<br> and other mammals.</p> <p> </p> <p>This upload is the transcriptome fasta file used for alignment for the dataset.</p>
Comprehensive large-scale datasets for 26 viral families for fine-tuning BERT-infect models
<p>These datasets were constructed in the paper "Hidden Challenges in Evaluating Spillover Risk of Zoonotic Viruses using Machine Learning Models" (doi: https://doi.org/10.1101/2024.04.25.591033). The details were also described in the git-hub (https://github.com/Junna-Kawasaki/BERT-infect_2024).</p> <ul> <li>The compressed files, such as ${virus}.tar.xz, contain fasta and genbank files.</li> </ul>
Data from: Viral transmission and infection prevalence in a cannibalistic host–pathogen system
<div> <div> <div> <div> <p>Cannibalism, while prevalent in the natural world, is often viewed as detrimental to a cannibal's health, especially when they consume pathogen-infected conspecifics. The argument stems from the idea that cannibalizing infected individuals increases the chance of coming into contact with a pathogen and subsequently becoming infected. Using an insect pest, the fall armyworm (<em>Spodoptera frugiperda</em>), that readily cannibalizes at the larval stage and its lethal pathogen, we experimentally examined how cannibalism affects viral transmission at both an individual and population level. Prior to death, the pathogen in the system stops the larval host from growing, resulting in infected individuals being smaller than healthy individuals. This leads to size-structured cannibalism of infected individuals with the larger healthy larvae consuming the smaller infected larvae, which is commonly observed. At the individual level, we show that the probability of cannibalism is relatively high for both infected and uninfected individuals especially when the cannibal is larger than the victim. However, the probability of the cannibal becoming infected given that a pathogen-infected individual has been cannibalized is relatively low. On a population level, when cannibalism is allowed to occur transmission rates decline. Additionally, by cannibalizing infected larvae, cannibals lower the infection risk for non-cannibals. Thus, cannibalism can decrease infection prevalence and, therefore, may not be as deleterious as once thought. Under certain circumstances, cannibalizing infected individuals, from the uninfected host's perspective, may even be advantageous, as one obtains a meal and decreases competition for resources with little chance of becoming infected.</p> </div> </div> </div> </div>
SomaScan dataset used to identify protein biomarkers for distinguishing between bacterial and viral infections in febrile children
<p>Protein profiles of children with confirmed bacterial infections (DB), confirmed viral infections (DV) in addition to healthy controls (HC). Protein profiles generated through the SomaScan 1.3k assay (SomaLogic, Colorado, USA).</p> <p>Data has been normalised already, including batch effect correction using COCONUT (https://cran.r-project.org/web/packages/COCONUT/COCONUT.pdf) and log2 transformed. </p> <p>Accompanying the protein abundance values is a separate .csv file containing information about the proteins, including UniProt ID and Entrez gene IDs associated with the proteins.</p>
LC-MS/MS plasma protein measurements from children with bacterial and viral infections - "MS-A"
<p>LC-MS/MS data generated from plasma samples from children with bacterial and viral infections. </p>
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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
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.