Skip to main content
Powered by ShareScore

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.

727

datasets available to search

ShareScore release 0.9.0

Reset

Dataset results

727 results for “Viral infections”

Learn how ShareScore rates datasets ↗
zenodo36/100

LC-MS/MS plasma protein measurements from children with bacterial and viral infections - "MS-B"

<p>LC-MS/MS data generated from plasma samples from children with bacterial and viral infections.&nbsp;</p>

openApr 2023View details →
dryad36/100

Data from: Hemin treatment drives viral reactivation and plasma cell differentiation of EBV latently infected B cells

<p>Epstein-Barr virus (EBV) and <em>Plasmodium falciparum</em> have a well described role in the development of endemic Burkitt lymphoma (BL), yet the mechanisms involved remain unknown. A major hallmark of malarial disease is hemolysis and bystander eryptosis of red blood cells, which causes release of free heme in large quantities into peripheral blood. We hypothesized that heme released during malaria infection drives differentiation of latently infected EBV-positive B cells, resulting in viral reactivation and release of infectious virus. To test this hypothesis, we used the EBV-positive Mutu I B-cell line and treated with hemin (the oxidized form of heme) and evaluated for evidence of EBV reactivation­. Hemin treatment resulted in the expression of EBV immediate early, early and late lytic gene transcripts. In addition, expression of CD138, a marker of plasma cells was co-expressed with the late lytic protein gp350 on hemin treated Mutu I cells. Finally, DNase-resistant EBV DNA indicative of virion production was detected in supernatant. To assess the transcriptional changes induced by hemin treatment, RNA sequencing was performed on mock- and hemin-treated Mutu I cells, and a shift from mature B cell transcripts to plasma cell transcripts was identified. To identify the mechanism of hemin-induced B cell differentiation, we measured levels of the plasma cell transcriptional repressor, BACH2, that contains specific heme binding sites. Hemin treatment caused significant degradation of BACH2 by 24 hours post-treatment in four BL cell lines (two EBV positive, two EBV negative). Knockdown of BACH2 in Mutu I cells using siRNAs significantly increased CD138+gp350+ cells to levels similar to treatment with hemin. This suggested that hemin induced BACH2 degradation was responsible for plasma cell differentiation and viral reactivation. Together, these data support a model where EBV reactivation can occur during malaria infection via heme modulation, providing a mechanistic link between malaria and EBV. </p>

opencc-zeroJul 2023View details →
zenodo36/100

Data for "Mixed viral infection constrains the genome formula of multipartite cucumber mosaic virus"

<p>We performed a study to assess the effect of mixed infection on the genome formula of multipartite virus CMV. We used qPCR to determine genome formulas and titer. Additionally, simulation models were developed to describe mechanisms for genome formula change under mixed infection.&nbsp;</p>

opencc-by-4.0Apr 2023View details →
ClinicalTrials.gov36/100

Study of Gefapixant (MK-7264) in Acute Cough for Participants With Induced Viral Upper Respiratory Tract Infection (URTI) (MK-7264-013)

ClinicalTrials.gov study NCT03569033. IPD Sharing: YES. Countries: 1. Publications: 1.

controlledIPD-YESFeb 2026View details →
ClinicalTrials.gov36/100

Wearable Assisted Viral Evidence (WAVE) Study A Decentralized, Prospective Study Exploring the Relationship Between Passively-collected Data From Wearable Activity Devices and Respiratory Viral Infect

ClinicalTrials.gov study NCT06207929. IPD Sharing: UNDECIDED. Countries: 1. Publications: 9.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Study of ALVR106 in Patients With Respiratory Viral Infections After Hematopoietic Cell and Solid Organ Transplant

ClinicalTrials.gov study NCT04933968. IPD Sharing: Not stated. Countries: 1. Publications: 2.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

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.

controlledIPD-YESFeb 2026View details →
ClinicalTrials.gov36/100

Effect of Addition of Raltegravir (MK-0518) to PI- or NNRTI-Based ART Regimens in HIV Infected Subjects With Undetectable Viral Load

ClinicalTrials.gov study NCT00515827. IPD Sharing: Not stated. Countries: 1. Publications: 5.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Efficacy of All-Oral Anti-Viral Therapy for Symptomatic Hepatitis C Virus Infection-Related Cryoglobulinemia

ClinicalTrials.gov study NCT02825212. IPD Sharing: NO. Countries: 1. Publications: 27.

closedIPD-NOFeb 2026View details →
ClinicalTrials.gov36/100

Evaluating the Safety and Efficacy of Romidepsin in Combination With Antiretroviral Therapy in HIV-Infected Adults With Suppressed Viral Load

ClinicalTrials.gov study NCT01933594. IPD Sharing: Not stated. Countries: 1. Publications: 3.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Effects of Chronic Viral Infection on Immune Response to Zoster Vaccination

ClinicalTrials.gov study NCT02590068. IPD Sharing: NO. Countries: 1. Publications: 22.

closedIPD-NOFeb 2026View details →
dryad36/100

Data from: Viral transmission and infection prevalence in a cannibalistic host–pathogen system

Open the record for dataset details and reuse information.

publicJan 2023View details →
dryad36/100

Data from: Hemin treatment drives viral reactivation and plasma cell differentiation of EBV latently infected B cells

Open the record for dataset details and reuse information.

publicAug 2023View details →
dryad32/100

Co-infection best predicts respiratory viral infection in a wild host

<p>1) The dynamics of directly transmitted pathogens in natural populations are likely to result from the combined effects of host traits, pathogen biology and interactions among pathogens within a host. Discovering how these factors work in concert to shape variation in pathogen dynamics in natural host – multi‐pathogen systems is fundamental to understanding population health.</p> <p>2) Here, we describe temporal variation in incidence and then elucidate the effect of hosts trait, season, and pathogen co‐occurrence on host infection risk using one of the most comprehensive studies of co‐infection in a wild population: a suite of seven directly‐transmitted, viral and bacterial, respiratory infections from a four‐year study of 200 free‐ranging African buffalo (<i>Syncerus caffer</i>).</p> <p>3) Incidence of upper respiratory infections was common throughout the study – five out of the seven pathogens appeared to be consistently circulating throughout our study population. One pathogen exhibited clear outbreak dynamics in our final study year and another was rarely detected.</p> <p>4) Co‐infection was also common in this system. The strongest indicator of pathogen occurrence for respiratory viruses was, in fact, the presence of other viral respiratory infections. Host traits had minimal effects on odds of pathogen occurrence but did modify pathogen‐pathogen associations. In contrast, only season predicted bacterial pathogen occurrence.</p> <p>5) Though a combination of environmental, behavioral, and physiological factors work together to shape disease dynamics, we found pathogen associations best determined infection risk. Our study demonstrates that, in absence of very fine‐scale data, the intricate changes among these factors are best represented by co‐infection.</p>

opencc-zeroDec 2020View details →
dryad32/100

Data from: Individual consumption of supplemental food as a predictor of reproductive performance and viral infection intensity

1.Supplemental food is often provided to threatened species in order to maintain or enhance reproductive fitness and thus population growth. However, its impact on individual reproductive fitness is rarely evaluated, despite being associated with both positive and negative consequences. 2. We used stable isotope analyses to characterise the relative proportional consumption of supplemental food and quantitative polymerase chain reaction (qPCR) to assess beak and feather disease viral infection intensity among parakeets. Life-history and nest-site data from a long-term monitoring effort was incorporated. 3. Older females benefitted the most from supplemental feeding; demonstrated by a greater reproductive uplift than younger females. There were no strong predictors of viral infection levels among nestlings. 4. Reproductive fitness, measured by the number of fledglings produced per brood, was positively associated with proportional dietary content of supplemental food among adult parakeets and breeding pairs that nested closer to feeding stations consumed more supplemental food than those nesting further away. 5. Synthesis and applications. Our study demonstrates that supplementary feeding can lead to an overall increase in population growth. However, by characterising individual consumption, we also reveal subtle patterns of use and differential benefits on reproductive fitness within a population. Manipulating the delivery of supplemental food may help to reduce demand on finite resources or target the proportion of a population that derives the most benefit, but is associated with trade-offs in fecundity. For example the use of, and access to feeding stations could potentially be targeted towards specific individuals or, positioned in the habitats most deficient in native food. However, increasing reproductive fitness in one component of the population may be accompanied by a decrease in another. This knowledge can be incorporated into adaptive management strategies that aim to fulfil specific objectives associated with species recovery and long-term viability as long as the relative importance of each objective is be considered.

opencc-zeroDec 2017View details →
dryad32/100

Data from: Exploring an alternative explanation for the second phase of viral decay: infection of short-lived cells in a drug-limited compartment during HAART

Most HIV-infected patients who initiate combination antiretroviral therapy experience a viral load decline in several phases. These phases are characterized by different rates of viral load decay that decrease when transitioning from one phase to the next. There is no consensus as to the origin of these phases. One hypothesis put forward is that short- and long-lived infected cells are responsible for the first and second phases of decay, respectively. However, significant differences in drug concentrations are observed in monocytes from various tissues, suggesting the first two phases of decay in viral loads could instead be attributed to short-lived cells being differently exposed to drugs. Compared to a well-exposed compartment, new cell infection can be expected in a compartment with limited drug exposure, thus leading to a slower viral load decay with potential virologic failure and drug resistance. In the current study, the latter hypothesis was investigated using a model of viral kinetics. Empirical datasets were involved in model elaboration and parameter estimation. In particular, susceptibility assay data was used for an in vitro to in vivo extrapolation based on the expected drug concentrations inside physiological compartments. Results from numerical experiments of the short-term evolution of viral loads can reproduce the first two phases of viral decay when allowing new short-lived cell infections in an unidentified drug-limited compartment. Model long-term predictions are however less consistent with clinical observations. For the hypothesis to hold, efavirenz, tenofovir and emtricitabine drug exposure in the drug-limited compartment would have to be very low compared to exposure in peripheral blood. This would lead to significant long-term viral growth and the frequent development of resistant strains, a prediction not supported by clinical observations. This suggests that the existence of a drug-limited anatomical compartment is unlikely, by itself, to explain the second phase of viral load decay.

opencc-zeroDec 2017View details →
zenodo32/100

Targeting host-virus interactions: In silico analysis of the binding of human milk oligosaccharides to viral proteins involved in respiratory infections

<p><span>Respiratory viral infections, a major public health concern, necessitate the continuous development of novel antiviral strategies, particularly in the face of emerging and re-emerging pathogens. In this study, we </span><span>explored</span><span> the potential of human milk oligosaccharides (HMOs) as broad-spectrum antiviral agents against key respiratory viruses. </span><span>By examining the</span><span> structural mimicry of host cell receptors and </span><span>their </span><span>known biological functions, including antiviral activities, we assessed the </span><span>ability</span><span> of HMOs to bind and potentially inhibit viral proteins crucial for host</span><span> </span><span>cell entry. Our <em>in silico</em> analysis </span><span>focused</span><span> on viral proteins integral to host-virus interactions</span><span>, namely,</span><span> the hemagglutinin protein of influenza, fusion proteins of respiratory syncytial and human metapneumovirus, and the spike protein of SARS-CoV-2. Using molecular docking and simulation studies, we </span><span>demonstrated</span><span> that HMOs exhibit varying binding affinities to these viral proteins, suggesting their potential as viral entry inhibitors. </span><span>This</span><span> study </span><span>identified</span><span> several HMOs with promising binding profiles, highlighting their potential in antiviral drug development. This research provides a foundation for utilizing HMOs as a natural source for designing new therapeutics, offering a novel approach in the fight against respiratory viral infections.</span></p>

opencc-by-4.0Dec 2023View details →
zenodo32/100

Removal of senescent cells reduces the viral load and attenuates pulmonary and systemic inflammation in SARS-CoV-2-infected, aged hamsters

<p>Older age is one of the strongest risk factors for coronavirus disease 2019 (COVID-19) morbidity and mortality. In an older adult, the chronic accumulation of senescent cells can interfere with the immune system and accentuate inflammation. Here, we sought to determine whether age-associated cellular senescence contributes to the severity of COVID-19 by studying the well-established golden hamster model of severe acute respiratory syndrome coronavirus (SARS-CoV-2)-driven lung disease. We found that aged hamsters (22 months of age) accumulate senescent cells in the lungs and that the senolytic drug ABT-263 (a Bcl-2-family inhibitor) depletes these cells at baseline and during a SARS-CoV-2 infection (when the senescent cell count is typically elevated). Relative to young hamsters (2 months of age), aged hamsters had a greater viral load during the acute phase of infection and displayed higher levels of fibrosis and worse body weight recovery during the post-acute phase. Interestingly, early treatment with ABT-263 was associated with a significantly lower pulmonary viral load and an amelioration of COVID-19-like lung disease in aged (but not young) animals. ABT-263 treatment of aged animals was also associated with lower pulmonary and systemic levels of senescence-associated secretory phenotype factors. We conclude that the removal of senescent cells via treatment with a senolytic reduces the pathologic severity of SARS-CoV-2 infection in aged hamsters. As several senolytics have recently moved into early-stage clinical trials, our present findings have clear clinical relevance.</p>

opencc-by-4.0Aug 2022View details →
zenodo32/100

Correlates of protection and viral load trajectories in omicron breakthrough infections in triple vaccinated healthcare workers

<p>Source data to figure 2-S1 and table S1 in manuscript entitled&nbsp;<strong><em>Correlates of protection and viral load trajectories in omicron breakthrough infections in triple vaccinated healthcare workers</em>, </strong>Nature Communications, 2023.<strong>&nbsp;</strong></p>

opencc-by-4.0Jan 2023View details →
ClinicalTrials.gov32/100

Clinical Application of PCR-based Diagnosis of Community-onset Viral Respiratory Infections.

ClinicalTrials.gov study NCT01133782. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →

ScienceDex guides

Understand access before you commit

These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.

Compare curated 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.

allen-brain-atlas
neuroscienceopenDocumentation, web resources, and API references are available online.
Last verified 2026-04-30Open record

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.

abode-home-cage
behavioral-neuroscienceopenThe DataShare record exposes download links for annotations, documentation, license text, and the zipped per-snippet data directory.
Last verified 2026-04-30Open record

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.

dandi-nwb
electrophysiologyopenPublished Dandiset metadata and archive endpoints are available through the production DANDI API.
Last verified 2026-04-30Open record

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.

ibl
behavioral-neuroscienceopenPublic sessions can be searched and loaded from the IBL public data server through ONE.
Last verified 2026-04-29Open record

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.

openneuro
neuroscienceopenPublished datasets are available on demand over the internet.
Last verified 2026-04-29Open record