ArticleVirology2011
IRF3 polymorphisms induce different innate anti-Theiler's virus immune responses in RAW264.7 macrophages.
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Susceptibility to Zika virus in a Collaborative Cross mouse strain is induced by Irf3 deficiency in vitro but requires other variants in vivo.PLoS pathogens · 2023Article
- Interferon regulatory factor 3 plays a role in macrophage responses to interferon-γ.Immunobiology · 2019Article
- Facets of Theiler's Murine Encephalomyelitis Virus-Induced Diseases: An Update.International journal of molecular sciences · 2019Review
- Activation of IRF3 contributes to IFN-γ and ISG54 expression during the immune responses to B16F10 tumor growth.International immunopharmacology · 2017Article
- Interferon-stimulated genes-essential antiviral effectors implicated in resistance to Theiler's virus-induced demyelinating disease.Journal of neuroinflammation · 2015Article
- Generation of replication-proficient influenza virus NS1 point mutants with interferon-hyperinducer phenotype.PloS one · 2014Article
- Distinct immune response in two MERS-CoV-infected patients: can we go from bench to bedside?PloS one · 2014Article
- IRF3 helps control acute TMEV infection through IL-6 expression but contributes to acute hippocampus damage following TMEV infection.Virus research · 2013Article
- Control of early Theiler's murine encephalomyelitis virus replication in macrophages by interleukin-6 occurs in conjunction with STAT1 activation and nitric oxide production.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Persistent viral infections can lead to disease such as myocarditis. Theiler's murine encephalomyelitis virus (TMEV) infects macrophages of SJL/J (H-2s) mice establishing persistent infections leading to demyelinating disease. In contrast macrophages from B10.S (H-2s) mice clear TMEV. Activation of the transcription factor IRF3 induces IFNβ, ISG56, and apoptosis for viral clearance, but also inflammatory cytokines, such as IL-23 and IL6, which contribute to disease. Here we identify polymorphisms in the IRF3 of SJL/J versus B10.S mice that are located in DNA binding, nuclear localization, and autoinhibitory domains. SJL-IRF3 expression in RAW264.7 macrophage cells with or without TMEV infection decreased IL-23p19 promoter activity compared with B10S-IRF3. In contrast SJL-IRF3 increased IL-6, ISG56 and IFNβ in response to TMEV. B10S-IRF3 expression augmented apoptotic caspase activation and decreased viral RNA in TMEV-infected macrophages while SJL-IRF3 increased viral replication with less caspase activation. Therefore IRF3 polymorphisms contribute to viral persistence and altered cytokine expression.
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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.