ArticleJournal of virology2013
Role of interferon regulatory factor 3-mediated apoptosis in the establishment and maintenance of persistent infection by Sendai virus.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Targeting pattern recognition receptors for cancer therapy: Mechanisms and strategies.Acta pharmaceutica Sinica. B · 2025Review
- PBLD promotes IRF3 mediated the type I interferon (IFN-I) response and apoptosis to inhibit viral replication.Cell death & disease · 2024Article
- Zinc-finger CCHC-type containing protein 8 promotes RNA virus replication by suppressing the type-I interferon responses.Journal of virology · 2024Article
- STING dependent BAX-IRF3 signaling results in apoptosis during late-stage Coxiella burnetii infection.Cell death & disease · 2024Article
- IRF3 inhibits nuclear translocation of NF-κB to prevent viral inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- Article
- Foot-and-Mouth Disease Virus Capsid Protein VP1 Antagonizes TPL2-Mediated Activation of the IRF3/IFN-β Signaling Pathway to Facilitate the Virus Replication.Frontiers in immunology · 2020Article
- Innate Immunity to Enteric Hepatitis Viruses.Cold Spring Harbor perspectives in medicine · 2019Review
- Identification of key genes and signaling pathways during Sendai virus infection in vitro.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2019Article
- Interferon regulatory factors 3 and 7 have distinct roles in the pathogenesis of alphavirus encephalomyelitis.The Journal of general virology · 2019Article
- Quantification of Infectious Sendai Virus Using Plaque Assay.Bio-protocol · 2018Article
- Sendai Virus Propagation Using Chicken Eggs.Bio-protocol · 2018Article
- Vibrio vulnificus quorum-sensing molecule cyclo(Phe-Pro) inhibits RIG-I-mediated antiviral innate immunity.Nature communications · 2018Article
- A new mechanism of interferon's antiviral action: Induction of autophagy, essential for paramyxovirus replication, is inhibited by the interferon stimulated gene, TDRD7.PLoS pathogens · 2018Article
- Establishment of a Human Cell Line Persistently Infected with Sendai Virus.Bio-protocol · 2017Article
- RIG-I-like receptor-induced IRF3 mediated pathway of apoptosis (RIPA): a new antiviral pathway.Protein & cell · 2017Review
- Endoplasmic Reticulum Stress-induced Hepatocellular Death Pathways Mediate Liver Injury and Fibrosis via Stimulator of Interferon Genes.The Journal of biological chemistry · 2016Article
- Ubiquitination of the Transcription Factor IRF-3 Activates RIPA, the Apoptotic Pathway that Protects Mice from Viral Pathogenesis.Immunity · 2016Article
- Response of Mammalian Macrophages to Challenge with the Chlorovirus Acanthocystis turfacea Chlorella Virus 1.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Infection of cultured cells by paramyxoviruses causes cell death, mediated by a newly discovered apoptotic pathway activated by virus infection. The key proapoptotic protein in this pathway is interferon regulatory factor 3 (IRF-3), which upon activation by virus infection binds BAX, translocates it to mitochondria, and triggers apoptosis. When IRF-3-knockdown cells were infected with Sendai virus (SeV), persistent infection (PI) was established. The PI cells produced infectious SeV continuously and constitutively expressed many innate immune genes. Interferon signaling was blocked in these cells. The elevated levels of IRF-3-driven genes in the PI cells indicated that the amount of residual IRF-3 activated by endogenous SeV was high enough to drive the transcriptional effects of IRF-3 but too low to trigger its apoptotic activity. We confirmed this IRF-3 threshold idea by generating a tetracycline (Tet)-inducible cell line for IRF-3 expression, which enabled us to express various levels of IRF-3. PI could be established in the Tet-off cell line, and as expected, when doxycycline was withdrawn, the cells underwent apoptosis. Finally, we tested for PI establishment in 12 mouse embryo fibroblasts by natural selection. Eleven lines became persistently infected; although seven out of them had low IRF-3 levels, four did not. When one of the latter four was further analyzed, we observed that it expressed a very low level of caspase 3, the final executor protease of the apoptotic pathway. These results demonstrated that SeV PI can arise from infection of normal wild-type cells, but only if they can find a way to impair the IRF-3-dependent apoptotic pathway.
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