ArticleNature structural & molecular biology2018
Influenza virus infection causes global RNAPII termination defects.
Article in Nature structural & molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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.
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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.
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Who cites it
42 citing papers in PubMed, 60 citations in OpenAlex.
- Divergent pathogenic mechanisms of influenza A and influenza B viruses.Archives of microbiology · 2026Review
- Review
- The Goldilocks state of transcriptional readthrough for chimeric splicing.Transcription · 2026Review
- Coordinating mRNA maturation: The U1 relay model.Molecular cell · 2026Review
- Isoforms in action: The impact of transcript diversity in phenotype.Genetics and molecular biology · 2026Article
- The Incoming Influenza Genome Assembles a Host RBP Network that Orchestrates Viral RNA Synthesis.bioRxiv : the preprint server for biology · 2025Article
- Influenza A virus NS1 suppresses nuclear speckles promoted gene expression by inhibition of transcription.Npj viruses · 2025Article
- Nonstructural Protein 1 of Influenza A (NS1A) Demonstrates Strain-Specific dsRNA Binding Capabilities.ACS infectious diseases · 2025Article
- Nuclear AGO2 supports influenza A virus replication through type-I interferon regulation.Nucleic acids research · 2025Article
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
- Epstein-Barr virus induces host shutoff extensively via BGLF5-independent mechanisms.Cell reports · 2024Article
- The host RNA polymerase II C-terminal domain is the anchor for replication of the influenza virus genome.Nature communications · 2024Article
- Isoginkgetin and Madrasin are poor splicing inhibitors.PloS one · 2024Article
- Influenza A virus replicates productively in primary human kidney cells and induces factors and mechanisms related to regulated cell death and renal pathology observed in virus-infected patients.Frontiers in cellular and infection microbiology · 2024Article
- Transcriptomic Profiling of Influenza A Virus-Infected Mouse Lung at Recovery Stage Using RNA Sequencing.Viruses · 2023Article
- RNA polymerase II CTD is dispensable for transcription and required for termination in human cells.EMBO reports · 2023Article
- mRNA 3'UTR lengthening by alternative polyadenylation attenuates inflammatory responses and correlates with virulence of Influenza A virus.Nature communications · 2023Article
- Cut site preference allows influenza A virus PA-X to discriminate between host and viral mRNAs.Nature microbiology · 2023Article
- 3'-End Processing of Eukaryotic mRNA: Machinery, Regulation, and Impact on Gene Expression.Annual review of biochemistry · 2023Review
- Stress-induced transcriptional readthrough into neighboring genes is linked to intron retention.iScience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
33 authors at 10 institutions in 5 countries.
Funding
Abstract
Viral infection perturbs host cells and can be used to uncover regulatory mechanisms controlling cellular responses and susceptibility to infections. Using cell biological, biochemical, and genetic tools, we reveal that influenza A virus (IAV) infection induces global transcriptional defects at the 3' ends of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions. Deregulated RNAPII leads to expression of aberrant RNAs (3' extensions and host-gene fusions) that ultimately cause global transcriptional downregulation of physiological transcripts, an effect influencing antiviral response and virulence. This phenomenon occurs with multiple strains of IAV, is dependent on influenza NS1 protein, and can be modulated by SUMOylation of an intrinsically disordered region (IDR) of NS1 expressed by the 1918 pandemic IAV strain. Our data identify a strategy used by IAV to suppress host gene expression and indicate that polymorphisms in IDRs of viral proteins can affect the outcome of an infection.
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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.