ArticleJournal of virology2012
A single-amino-acid polymorphism in reovirus protein μ2 determines repression of interferon signaling and modulates myocarditis.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
38 citing papers in PubMed, 52 citations in OpenAlex.
- Identification of reovirus reassortants with enhanced oncolytic activity in human fibrosarcoma cells.Virus genes · 2026Article
- Reovirus µ2 residue 208 drives SRSF2-dependent nuclear hyperaccumulation of IRF9.microPublication biology · 2026Article
- 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
- Cell Killing by Reovirus: Mechanisms and Consequences.Current topics in microbiology and immunology · 2023Review
- Reovirus μ2 Protein Impairs Translation to Reduce U5 snRNP Protein Levels.International journal of molecular sciences · 2022Article
- The μ2 and λ1 Proteins of Mammalian Reovirus Modulate Early Events Leading to Induction of the Interferon Signaling Network.Viruses · 2022Article
- Reovirus Efficiently Reassorts Genome Segments during Coinfection and Superinfection.Journal of virology · 2022Article
- Reovirus μ2 protein modulates host cell alternative splicing by reducing protein levels of U5 snRNP core components.Nucleic acids research · 2022Article
- The M2 Gene Is a Determinant of Reovirus-Induced Myocarditis.Journal of virology · 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
- The reovirus μ2 C-terminal loop inversely regulates NTPase and transcription functions versus binding to factory-forming μNS and promotes replication in tumorigenic cells.Journal of virology · 2021Article
- Article
- Reovirus σ3 Protein Limits Interferon Expression and Cell Death Induction.Journal of virology · 2020Article
- Mammalian orthoreovirus core protein μ2 reorganizes host microtubule-organizing center components.Virology · 2020Article
- Polymorphisms in the Most Oncolytic Reovirus Strain Confer Enhanced Cell Attachment, Transcription, and Single-Step Replication Kinetics.Journal of virology · 2020Article
- Viral modulation of cellular RNA alternative splicing: A new key player in virus-host interactions?Wiley interdisciplinary reviews. RNA · 2019Review
- RNA regulatory processes in RNA virus biology.Wiley interdisciplinary reviews. RNA · 2019Review
- How Many Mammalian Reovirus Proteins are involved in the Control of the Interferon Response?Pathogens (Basel, Switzerland) · 2019Review
- Piscine orthoreovirus subtype 3 (PRV-3) causes heart inflammation in rainbow trout (Oncorhynchus mykiss).Veterinary research · 2019Article
- Reovirus-Induced Apoptosis in the Intestine Limits Establishment of Enteric Infection.Journal of virology · 2018Article
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 2 institutions in 1 country.
Funding
Abstract
Myocarditis is indicated as the second leading cause of sudden death in young adults. Reovirus induces myocarditis in neonatal mice, providing a tractable model system for investigation of this important disease. Alpha/beta-interferon (IFN-α/β) treatment improves cardiac function and inhibits viral replication in patients with chronic myocarditis, and the host IFN-α/β response is a determinant of reovirus strain-specific differences in induction of myocarditis. Virus-induced IFN-β stimulates a signaling cascade that establishes an antiviral state and further induces IFN-α/β through an amplification loop. Reovirus strain-specific differences in induction of and sensitivity to IFN-α/β are associated with the viral M1, L2, and S2 genes. The reovirus M1 gene-encoded μ2 protein is a strain-specific repressor of IFN-β signaling, providing one possible mechanism for the variation in resistance to IFN and induction of myocarditis between different reovirus strains. We report here that μ2 amino acid 208 determines repression of IFN-β signaling and modulates reovirus induction of IFN-β in cardiac myocytes. Moreover, μ2 amino acid 208 determines reovirus replication, both in initially infected cardiac myocytes and after viral spread, by regulating the IFN-β response. Amino acid 208 of μ2 also influences the cytopathic effect in cardiac myocytes after spread. Finally, μ2 amino acid 208 modulates myocarditis in neonatal mice. Thus, repression of IFN-β signaling mediated by reovirus μ2 amino acid 208 is a determinant of the IFN-β response, viral replication and damage in cardiac myocytes, and myocarditis. These results demonstrate that a single amino acid difference between viruses can dictate virus strain-specific differences in suppression of the host IFN-β response and, consequently, damage to the heart.
Indexed as
Identifiers
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.