ArticleThe Journal of general virology2017
Single-cell studies of IFN-β promoter activation by wild-type and NS1-defective influenza A viruses.
Article in The Journal of general virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Pooled it
- Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state.Cell systems · 2026Article
- Live-cell single-vRNP imaging identifies viral gene expression signatures that shape influenza infection heterogeneity.Cell systems · 2026Article
- Interferon-β induction heterogeneity during KSHV infection is correlated to levels and activation of the transcription factors ATF2 and RelA, and not IRF3.PLoS pathogens · 2026Article
- Intrinsic OASL expression governs heterogeneity in interferon induction during influenza A virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state.bioRxiv : the preprint server for biology · 2025Article
- Interferon-β induction heterogeneity during KSHV infection is correlated to levels and activation of the transcription factors ATF2 and RelA, and not IRF3.bioRxiv : the preprint server for biology · 2025Article
- Seasonal influenza a virus lineages exhibit divergent abilities to antagonize interferon induction and signaling.PLoS pathogens · 2024Article
- Maximal interferon induction by influenza lacking NS1 is infrequent owing to requirements for replication and export.PLoS pathogens · 2023Article
- Comprehensive single cell analysis of pandemic influenza A virus infection in the human airways uncovers cell-type specific host transcriptional signatures relevant for disease progression and pathogenesis.Frontiers in immunology · 2022Article
- Library-based analysis reveals segment and length dependent characteristics of defective influenza genomes.PLoS pathogens · 2021Article
- Elevated temperature inhibits SARS-CoV-2 replication in respiratory epithelium independently of IFN-mediated innate immune defenses.PLoS biology · 2021Article
- Epigenetic and transcriptional control of interferon-β.The Journal of experimental medicine · 2021Article
- Viral and host heterogeneity and their effects on the viral life cycle.Nature reviews. Microbiology · 2021Review
- Constitutive TRIM22 Expression in the Respiratory Tract Confers a Pre-Existing Defence Against Influenza A Virus Infection.Frontiers in cellular and infection microbiology · 2021Article
- Single cell resolution of SARS-CoV-2 tropism, antiviral responses, and susceptibility to therapies in primary human airway epithelium.PLoS pathogens · 2021Article
- Viral Subpopulation Screening Guides in Designing a High Interferon-Inducing Live Attenuated Influenza Vaccine by Targeting Rare Mutations in NS1 and PB2 Proteins.Journal of virology · 2020Article
- Virus-Intrinsic Differences and Heterogeneous IRF3 Activation Influence IFN-Independent Antiviral Protection.iScience · 2020Article
- Cellular co-infection can modulate the efficiency of influenza A virus production and shape the interferon response.PLoS pathogens · 2020Article
- Cell type- and replication stage-specific influenza virus responses in vivo.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Deletion or truncation of NS1, the principal IFN antagonist of influenza viruses, leads to increased IFN induction during influenza virus infection. We have studied activation of the IFN induction cascade by both wild-type and NS1-defective viruses at the single-cell level using a cell line expressing GFP under the control of the IFN-β promoter and by examining MxA expression. The IFN-β promoter was not activated in all infected cells even during NS1-defective virus infections. Loss of NS1 expression is therefore insufficient per se to induce IFN in an infected cell, and factors besides NS1 expression status must dictate whether the IFN response is activated. The IFN response was efficiently stimulated in these cells following infection with other viruses; the differential IFN response we observe with influenza viruses is therefore not cell specific but is likely due to differences in the nature of the infecting virus particles and their subsequent replication.
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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.