ArticleeLife2020
Type I interferon underlies severe disease associated with Junín virus infection in mice.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 19 citations in OpenAlex.
- Junín virus and Argentine haemorrhagic fever: Virology, pathogenesis, diagnosis, and prevention strategies.World journal of virology · 2026Review
- The Role of Human Viral Entry Receptor Mouse Models in Advancing Antiviral Antibodies and Vaccines.Vaccines · 2026Review
- Efficacy of an Fc-silent antibody targeting the apical domain of human transferrin receptor 1 in transgenic mouse models of Junín virus infection.Antiviral research · 2026Article
- Going wild: prioritizing experimental models of rodent-borne viruses to decode zoonotic spillover and pandemic risk.Journal of virology · 2026Review
- Computer-Aided Discovery of Small-Molecule Inhibitors of Pathogenic New World Arenavirus Entry and Replication.ACS infectious diseases · 2026Article
- A Transgenic Syrian Hamster Model for New World Hemorrhagic Fever Mammarenavirus Infection.Research square · 2026Article
- In situ insights into antibody-mediated neutralization of a pre-fusion Junin virus glycoprotein complex.Cell reports · 2025Article
- Animal Models of Pathogenic New World Arenaviruses.Microorganisms · 2025Review
- A novel neutralizing antibody recognizing a conserved conformational epitope in PDCoV S1 protein and its therapeutic efficacy in piglets.Journal of virology · 2025Article
- Discovery and biological confirmation of a highly divergent Tacaribe virus in metatranscriptomic data from neotropical bats.mSphere · 2024Article
- Vascular dysfunction in hemorrhagic viral fevers: opportunities for organotypic modeling.Biofabrication · 2024Review
- Restoration of virulence in the attenuated Candid#1 vaccine virus requires reversion at both positions 168 and 427 in the envelope glycoprotein GPC.Journal of virology · 2024Article
- Alternative translation contributes to the generation of a cytoplasmic subpopulation of the Junín virus nucleoprotein that inhibits caspase activation and innate immunity.Journal of virology · 2024Article
- Entry inhibitors as arenavirus antivirals.Frontiers in microbiology · 2024Review
- The Arenaviridae Family: Knowledge Gaps, Animal Models, Countermeasures, and Prototype Pathogens.The Journal of infectious diseases · 2023Article
- A dsRNA-binding mutant reveals only a minor role of exonuclease activity in interferon antagonism by the arenavirus nucleoprotein.PLoS pathogens · 2023Article
- Host receptor-targeted therapeutic approach to counter pathogenic New World mammarenavirus infections.Nature communications · 2022Article
- The board is set, the pieces are moving: Modulation of New World arenavirus entry by host proteins.PLoS pathogens · 2021Review
- Glycoprotein N-linked glycans play a critical role in arenavirus pathogenicity.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Junín virus (JUNV) is one of five New World mammarenaviruses (NWMs) that causes fatal hemorrhagic disease in humans and is the etiological agent of Argentine hemorrhagic fever (AHF). The pathogenesis underlying AHF is poorly understood; however, a prolonged, elevated interferon-α (IFN-α) response is associated with a negative disease outcome. A feature of all NWMs that cause viral hemorrhagic fever is the use of human transferrin receptor 1 (hTfR1) for cellular entry. Here, we show that mice expressing hTfR1 develop a lethal disease course marked by an increase in serum IFN-α concentration when challenged with JUNV. Further, we provide evidence that the type I IFN response is central to the development of severe JUNV disease in hTfR1 mice. Our findings identify hTfR1-mediated entry and the type I IFN response as key factors in the pathogenesis of JUNV infection in mice.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.