ArticleJournal of virology2010
Interferon regulatory factor 3 attenuates reovirus myocarditis and contributes to viral clearance.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 43 citations in OpenAlex.
- SAMD9 senses cytosolic double-stranded nucleic acids in epithelial and mesenchymal cells to induce antiviral immunity.Nature communications · 2025Article
- Infectious factors in myocarditis: a comprehensive review of common and rare pathogens.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- Lymph node sharing between pancreas, gut, and liver leads to immune crosstalk and regulation of pancreatic autoimmunity.Immunity · 2023Article
- Cell Killing by Reovirus: Mechanisms and Consequences.Current topics in microbiology and immunology · 2023Review
- Early Events in Reovirus Infection Influence Induction of Innate Immune Response.Journal of virology · 2022Article
- The Reovirus σ3 Protein Inhibits NF-κB-Dependent Antiviral Signaling.Journal of virology · 2022Article
- A CRISPR-Cas9 screen reveals a role for WD repeat-containing protein 81 (WDR81) in the entry of late penetrating viruses.PLoS pathogens · 2022Article
- The multi-functional reovirus σ3 protein is a virulence factor that suppresses stress granule formation and is associated with myocardial injury.PLoS pathogens · 2021Article
- Review
- Myocarditis in Humans and in Experimental Animal Models.Frontiers in cardiovascular medicine · 2019Review
- Cardioimmunology: the immune system in cardiac homeostasis and disease.Nature reviews. Immunology · 2018Review
- Differential Delivery of Genomic Double-Stranded RNA Causes Reovirus Strain-Specific Differences in Interferon Regulatory Factor 3 Activation.Journal of virology · 2018Article
- Current understanding of reovirus oncolysis mechanisms.Oncolytic virotherapy · 2018Review
- Reovirus infection induces stabilization and up-regulation of cellular transcripts that encode regulators of TGF-β signaling.PloS one · 2018Article
- Spontaneous activation of a MAVS-dependent antiviral signaling pathway determines high basal interferon-β expression in cardiac myocytes.Journal of molecular and cellular cardiology · 2017Article
- Reovirus inhibits interferon production by sequestering IRF3 into viral factories.Scientific reports · 2017Article
- The Orchestra of Reovirus Cell Entry.Current clinical microbiology reports · 2017Article
- Viral RNA at Two Stages of Reovirus Infection Is Required for the Induction of Necroptosis.Journal of virology · 2017Article
- NF-κB activation is cell type-specific in the heart.Virology · 2017Article
- Diminished reovirus capsid stability alters disease pathogenesis and littermate transmission.PLoS pathogens · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Apoptosis is a pathological hallmark of encephalitis and myocarditis caused by reovirus in newborn mice. In cell culture models, the antiviral transcription factor interferon regulatory factor 3 (IRF-3) enhances reovirus-induced apoptosis following activation via retinoic acid inducible gene I and interferon promoter-stimulating factor 1. To determine the role of IRF-3 in reovirus disease, we infected newborn IRF-3(+/+) and IRF-3(-/-) mice perorally with mildly virulent strain type 1 Lang (T1L) and fully virulent strain type 3 SA+ (T3SA+) and monitored infected animals for survival. Both wild-type and IRF-3(-/-) mice succumbed with equivalent frequencies to infection with T3SA+. However, the absence of IRF-3 was associated with significantly decreased survival rates following infection with T1L. The two virus strains achieved similar peak titers in IRF-3(+/+) and IRF-3(-/-) mice in the intestine, brain, heart, liver, and spleen. However, by day 12 postinoculation, titers in all organs examined were 10- to 100-fold higher in IRF-3(-/-) mice than those in wild-type mice. Increased titers were associated with marked pathological changes in all organs examined, especially in the heart, where absence of IRF-3 resulted in severe myocarditis. Cellular and humoral immune responses were equivalent in wild-type and IRF-3(-/-) animals, suggesting that IRF-3 functions independently of the adaptive immune response to enhance reovirus clearance. Thus, IRF-3 serves to facilitate virus clearance and prevent tissue injury in response to reovirus infection.
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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.