ArticleJournal of virology2019
Influenza A Virus Utilizes Low-Affinity, High-Avidity Interactions with the Nuclear Import Machinery To Ensure Infection and Immune Evasion.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Identifying a novel region in the Tembusu virus NS5 protein antagonizing type I interferon signaling.Journal of virology · 2025Article
- Mechanisms of miR-18a-5p Target NEDD9-Mediated Suppression of H5N1 Influenza Virus in Mammalian and Avian Hosts.Veterinary sciences · 2025Article
- Two Phylogenetic Cohorts of the Nucleocapsid Protein NP and Their Correlation with the Host Range of Influenza A Viruses.Doklady. Biochemistry and biophysics · 2024Article
- Nonmuscle myosin IIA promotes the internalization of influenza A virus and regulates viral polymerase activity through interacting with nucleoprotein in human pulmonary cells.Virologica Sinica · 2023Article
- A rapid and efficient platform for antiviral crRNA screening using CRISPR-Cas13a-based nucleic acid detection.Frontiers in immunology · 2023Article
- Interactions between Influenza A Virus Nucleoprotein and Gene Segment Untranslated Regions Facilitate Selective Modulation of Viral Gene Expression.Journal of virology · 2022Article
- Domain in Fiber-2 interacted with KPNA3/4 significantly affects the replication and pathogenicity of the highly pathogenic FAdV-4.Virulence · 2021Article
- An Inside Job: Applications of Intracellular Single Domain Antibodies.Biomolecules · 2020Review
- Exploring cellular biochemistry with nanobodies.The Journal of biological chemistry · 2020Review
- Applying Antibodies Inside Cells: Principles and Recent Advances in Neurobiology, Virology and Oncology.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2020Review
- Differential Behaviours and Preferential Bindings of Influenza Nucleoproteins on Importins-α.Viruses · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The incoming influenza A virus (IAV) genome must pass through two distinct barriers in order to establish infection in the cell: the plasma membrane and the nuclear membrane. A precise understanding of the challenges imposed by the nuclear barrier remains outstanding. Passage across is mediated by host karyopherins (KPNAs), which bind to the viral nucleoprotein (NP) via its N-terminal nuclear localization sequence (NLS). The binding affinity between the two molecules is low, but NP is present in a high copy number, which suggests that binding avidity plays a compensatory role during import. Using nanobody-based technology, we demonstrate that a high binding avidity is required for infection, though the absolute value differs between cell types and correlates with their relative susceptibility to infection. In addition, we demonstrate that increasing the affinity level caused a decrease in avidity requirements for some cell types but blocked infection in others. Finally, we show that genomes that become frustrated by low avidity and remain cytoplasmic trigger the type I interferon response. Based on these results, we conclude that IAV balances affinity and avidity considerations in order to overcome the nuclear barrier across a broad range of cell types. Furthermore, these results provide evidence to support the long-standing hypothesis that IAV's strategy of import and replication in the nucleus facilitates immune evasion.
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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.