ArticleViruses2025
Deficiency of IFNAR1 Increases the Production of Influenza Vaccine Viruses in MDCK Cells.
Article in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
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
3 citing papers in PubMed.
- Development of a pandemic H5N1 influenza vaccine using MDCK suspension cells: A scalable and efficient production platform.Human vaccines & immunotherapeutics · 2026Article
- Screening of Low-Tumorigenic MDCK Cells for Potential Influenza Vaccine Substrates and Transcriptomic Analyses.International journal of molecular sciences · 2026Article
- Molecular, Functional, and Ecological Characterization of Antarctic Penguin Orthoavulaviruses (AVV17-19).Animals : an open access journal from MDPI · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Cell culture-based influenza vaccines exhibit comparable safety and immunogenicity to traditional egg-based vaccines. However, improving viral yield remains a key challenge in optimizing cell culture-based production systems. Madin-Darby canine kidney (MDCK) cells, the predominant cell line for influenza vaccine production, inherently activate interferon (IFN)-mediated antiviral defenses that restrict viral replication. To overcome this limitation, we employed CRISPR/Cas9 gene-editing technology to generate an IFN alpha/beta receptor subunit 1 (IFNAR1)-knockout (KO) adherent MDCK cell line. Viral titer analysis demonstrated significant enhancements in the yield of multiple vaccine strains (H1N1, H3N2, and type B) in IFNAR1-KO cells compared to wild-type (WT) cells. Transcriptomic profiling revealed marked downregulation of key interferon-stimulated genes (ISGs)-including
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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.