ArticleFrontiers in immunology2018
Influenza A Virus Facilitates Its Infectivity by Activating p53 to Inhibit the Expression of Interferon-Induced Transmembrane Proteins.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Systematic review and meta-analysis of genome-wide pooled CRISPR screens to identify host factors involved in influenza A virus infection.Journal of virology · 2024Pooled it
- Interferon-induced transmembrane proteins: membrane gatekeepers of fusion and infection.Frontiers in cellular and infection microbiology · 2026Review
- Exploring the role of the key gene TNFAIP3 between periodontitis and influenza A through bioinformatic analysis and molecular docking.PloS one · 2026Article
- The puzzling regulation of the interferon signaling system by the p53 tumor suppressor protein.Cellular and molecular life sciences : CMLS · 2025Article
- Nuclear AGO2 supports influenza A virus replication through type-I interferon regulation.Nucleic acids research · 2025Article
- Preventing occludin tight-junction disruption via inhibition of microRNA-193b-5p attenuates viral load and influenza-induced lung injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- The Wheel of p53 Helps to Drive the Immune System.International journal of molecular sciences · 2023Review
- Differential Leukocyte Expression ofJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Article
- De Novo Assembly of 20 Chicken Genomes Reveals the Undetectable Phenomenon for Thousands of Core Genes on Microchromosomes and Subtelomeric Regions.Molecular biology and evolution · 2022Article
- Application of the CRISPR/Cas9 System to Study Regulation Pathways of the Cellular Immune Response to Influenza Virus.Viruses · 2022Review
- The CCR5 Gene Edited CD34Frontiers in immunology · 2022Article
- Adaptive homeostasis and the p53 isoform network.EMBO reports · 2021Review
- Induction and Evasion of Type-I Interferon Responses during Influenza A Virus Infection.Cold Spring Harbor perspectives in medicine · 2021Review
- Elucidating the Effects of Curcumin against Influenza Using In Silico and In Vitro Approaches.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Review
- p53 loss activates prometastatic secretory vesicle biogenesis in the Golgi.Science advances · 2021Article
- Review
- Comprehensive Transcriptomic Analysis Identifies Novel Antiviral Factors Against Influenza A Virus Infection.Frontiers in immunology · 2021Article
- Article
- p53 promotes ZDHHC1-mediated IFITM3 palmitoylation to inhibit Japanese encephalitis virus replication.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human influenza virus (IAV) are among the most common pathogens to cause human respiratory infections. A better understanding on interplay between IAV and host factors may provide clues for disease prevention and control. While many viruses are known to downregulate p53 upon entering the cell to reduce the innate host antiviral response, IAV infection is unusual in that it activates p53. However, it has not been clear whether this process has proviral or antiviral effects. In this study, using human isogenic p53 wild-type and p53null A549 cells generated from the CRISPR/Cas9 technology, we observed that p53null cells exhibit significantly reduced viral propagation when infected with influenza A virus (strain A/Puerto Rico/8/1934 H1N1). Genome-wide microarray analysis revealed that p53 regulates the expression of a large set of interferon-inducible genes, among which the interferon-induced transmembrane family members IFITM1, IFITM2, and IFITM3 were most significantly downregulated by the expression of p53. Knockdown of interferon-induced transmembrane proteins (IFITMs) by short interfering RNAs enhanced influenza virus infectivity in p53null A549 cells, while overexpressed IFITMs in A549 cells blocked virus entry. Intriguingly, regulation of IFITMs by p53 is independent of its transcriptional activity, as the p53 short isoform Δ40p53 recapitulates IFITM regulation. Taken together, these data reveal that p53 activation by IAV is an essential step in maintaining its infectivity. This novel association between human p53 and the broad spectrum antiviral proteins, the IFITMs, demonstrates a previous mechanism employed by influenza virus to enhance its propagation
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