ArticleProceedings of the National Academy of Sciences of the United States of America2007
Influenza virus targets the mRNA export machinery and the nuclear pore complex.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers.
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Who cites it
189 citing papers in PubMed, 281 citations in OpenAlex.
- A multimodaliScience · 2026Article
- Tripartite motif-containing 34 (TRIM34) protein interacts with the nucleocytoplasmic transport machinery and negatively modulates antiviral responses.PLoS pathogens · 2026Article
- Breaking barriers: Respiratory viral strategies targeting the host's nuclear pore complex and nuclear transport pathways.Molecular biology of the cell · 2026Review
- Human respiratory syncytial virus regulates the expression of interferon-stimulated genes through modulation of fibrillarin.Frontiers in cellular and infection microbiology · 2026Article
- Viral interference of nucleocytoplasmic transport.The Journal of biological chemistry · 2025Review
- Differential Host Responses and Viral Replication of Highly Pathogenic Avian Influenza H5N1 Strains in Diverse Cell Lines with a Raw Milk Supplement.Life (Basel, Switzerland) · 2025Article
- The Genetic Landscape of Acute Necrotizing Encephalopathy: Insights Into the Possible Pathogenesis.Journal of clinical neurology (Seoul, Korea) · 2025Article
- Structural mechanism of DDX39B regulation by human TREX-2 and a related complex in mRNP remodeling.Nature communications · 2025Article
- Influenza A virus RNA localisation and the interceding trafficking pathways of the host cell.PLoS pathogens · 2025Review
- Article
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- Seasonal influenza a virus lineages exhibit divergent abilities to antagonize interferon induction and signaling.PLoS pathogens · 2024Article
- Paramyxovirus matrix proteins modulate host cell translation via exon-junction complex interactions in the cytoplasm.bioRxiv : the preprint server for biology · 2024Article
- Zika virus NS5 protein inhibits type I interferon signaling via CRL3 E3 ubiquitin ligase-mediated degradation of STAT2.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- SARS-CoV-2 Nsp1 traps RNA in the nucleus to escape immune detection.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Unravelling the interaction between Influenza virus and the nuclear pore complex: insights into viral replication and host immune response.Virusdisease · 2024Review
- Inhibition of mRNA nuclear export promotes SARS-CoV-2 pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Influenza A virus NS1 effector domain is required for PA-X-mediated host shutoff in infected cells.Journal of virology · 2024Article
- Identifying cellular RNA-binding proteins during infection uncovers a role for MKRN2 in influenza mRNA trafficking.PLoS pathogens · 2024Article
- SARS-CoV-2 Orf6 is positioned in the nuclear pore complex by Rae1 to inhibit nucleocytoplasmic transport.Molecular biology of the cell · 2024Article
129 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The NS1 protein of influenza A virus is a major virulence factor that is essential for pathogenesis. NS1 functions to impair innate and adaptive immunity by inhibiting host signal transduction and gene expression, but its mechanisms of action remain to be fully elucidated. We show here that NS1 forms an inhibitory complex with NXF1/TAP, p15/NXT, Rae1/mrnp41, and E1B-AP5, which are key constituents of the mRNA export machinery that interact with both mRNAs and nucleoporins to direct mRNAs through the nuclear pore complex. Increased levels of NXF1, p15, or Rae1 revert the mRNA export blockage induced by NS1. Furthermore, influenza virus down-regulates Nup98, a nucleoporin that is a docking site for mRNA export factors. Reduced expression of these mRNA export factors renders cells highly permissive to influenza virus replication, demonstrating that proper levels of key constituents of the mRNA export machinery protect against influenza virus replication. Because Nup98 and Rae1 are induced by interferons, down-regulation of this pathway is likely a viral strategy to promote viral replication. These findings demonstrate previously undescribed influenza-mediated viral-host interactions and provide insights into potential molecular therapies that may interfere with influenza 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.