ArticlePLoS pathogens2019
Biphasic and cardiomyocyte-specific IFIT activity protects cardiomyocytes from enteroviral infection.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Enterovirus infections in children.Pediatric investigation · 2026Review
- Mutant CHCHD10 disrupts cytochrome c oxidation and activates mitochondrial retrograde signaling.EMBO molecular medicine · 2026Article
- Cardiomyocyte β-arrestins mediate inflammation and cGAS-STING activation in CVB3 viral myocarditis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Heart-specific NFAT5 knockout suppresses type I interferon signaling and aggravates coxsackievirus-induced myocarditis.Basic research in cardiology · 2024Article
- Article
- ADAM9 promotes type I interferon-mediated innate immunity during encephalomyocarditis virus infection.Nature communications · 2024Article
- Loss of TRIM29 mitigates viral myocarditis by attenuating PERK-driven ER stress response in male mice.Nature communications · 2024Article
- A Kaposi's sarcoma-associated herpes virus-encoded microRNA contributes to dilated cardiomyopathy.Signal transduction and targeted therapy · 2023Article
- IFN-Induced Protein with Tetratricopeptide Repeats 2 Limits Autoimmune Inflammation by Regulating Myeloid Cell Activation and Metabolic Activity.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Identified Three Interferon Induced Proteins as Novel Biomarkers of Human Ischemic Cardiomyopathy.International journal of molecular sciences · 2021Article
- Identification of key molecular markers of acute coronary syndrome using peripheral blood transcriptome sequencing analysis and mRNA-lncRNA co-expression network construction.Bioengineered · 2021Article
- IRF3-mediated pathogenicity in a murine model of human hepatitis A.PLoS pathogens · 2021Article
- Article
- Hepatocytes trap and silence coxsackieviruses, protecting against systemic disease in mice.Communications biology · 2020Article
- Protein modification with ISG15 blocks coxsackievirus pathology by antiviral and metabolic reprogramming.Science advances · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Viral myocarditis is a serious disease, commonly caused by type B coxsackieviruses (CVB). Here we show that innate immune protection against CVB3 myocarditis requires the IFIT (IFN-induced with tetratricopeptide) locus, which acts in a biphasic manner. Using IFIT locus knockout (IFITKO) cardiomyocytes we show that, in the absence of the IFIT locus, viral replication is dramatically increased, indicating that constitutive IFIT expression suppresses CVB replication in this cell type. IFNβ pre-treatment strongly suppresses CVB3 replication in wild type (wt) cardiomyocytes, but not in IFITKO cardiomyocytes, indicating that other interferon-stimulated genes (ISGs) cannot compensate for the loss of IFITs in this cell type. Thus, in isolated wt cardiomyocytes, the anti-CVB3 activity of IFITs is biphasic, being required for protection both before and after T1IFN signaling. These in vitro findings are replicated in vivo. Using novel IFITKO mice we demonstrate accelerated CVB3 replication in pancreas, liver and heart in the hours following infection. This early increase in virus load in IFITKO animals accelerates the induction of other ISGs in several tissues, enhancing virus clearance from some tissues, indicating that-in contrast to cardiomyocytes-other ISGs can offset the loss of IFITs from those cell types. In contrast, CVB3 persists in IFITKO hearts, and myocarditis occurs. Thus, cardiomyocytes have a specific, biphasic, and near-absolute requirement for IFITs to control CVB infection.
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.