ReviewViruses2018
Modulation of Innate Immune Responses by the Influenza A NS1 and PA-X Proteins.
Review in Viruses, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Plant-Derived Food Grade Substances (PDFGS) Active Against Respiratory Viruses: A Systematic Review of Non-clinical Studies.Frontiers in nutrition · 2021Pooled it
- Influenza-related Deaths in Young Children: Observations From a German Case Series.The Pediatric infectious disease journal · 2026Article
- Pre-existing and cross-reactive immunity to avian influenza H5N1 in humans: Implications for pandemic risk and vaccine strategies.The Journal of infection · 2026Review
- Dose-Dependent Alterations in Lung Immune Subpopulations in Influenza a Virus Infection.International journal of molecular sciences · 2026Article
- Molecular Insights into High-Pathogenicity RNA Viruses.Viruses · 2026Review
- Epidemiological and Genomic Characterization of H5 Subtype Avian Influenza Viruses in Jining City, 2024-2025.Pathogens (Basel, Switzerland) · 2026Article
- Tripartite motif-containing 34 (TRIM34) protein interacts with the nucleocytoplasmic transport machinery and negatively modulates antiviral responses.PLoS pathogens · 2026Article
- Article
- Impaired host shutoff is a fitness cost associated with baloxavir marboxil resistance mutations in influenza A virus PA/PA-X nuclease domain.PLoS pathogens · 2026Article
- The PA-X host shutoff site 100 V exerts a contrary effect on viral fitness of the highly pathogenic H7N9 influenza A virus in mice and chickens.Virulence · 2025Article
- Molecular and ecological determinants of mammalian adaptability in avian influenza virus.Infection · 2025Review
- The applications of live attenuated influenza a virus with modified NS1 gene.Molecular therapy. Nucleic acids · 2025Review
- Exploring genetic signatures of zoonotic influenza A virus at the swine-human interface with phylogenetic and ancestral sequence reconstruction.Virus evolution · 2025Article
- Seasonal influenza a virus lineages exhibit divergent abilities to antagonize interferon induction and signaling.PLoS pathogens · 2024Article
- Dual receptor-binding, infectivity, and transmissibility of an emerging H2N2 low pathogenicity avian influenza virus.Nature communications · 2024Article
- Opportunities and challenges for T cell-based influenza vaccines.Nature reviews. Immunology · 2024Review
- Evaluation of a novel intramuscular prime/intranasal boost vaccination strategy against influenza in the pig model.PLoS pathogens · 2024Article
- Molecular Markers and Mechanisms of Influenza A Virus Cross-Species Transmission and New Host Adaptation.Viruses · 2024Review
- Changes in the Expression of Proteins Associated with Neurodegeneration in the Brains of Mice after Infection with Influenza A Virus with Wild Type and Truncated NS1.International journal of molecular sciences · 2024Article
- Antiviral responses versus virus-induced cellular shutoff: a game of thrones between influenza A virus NS1 and SARS-CoV-2 Nsp1.Frontiers in cellular and infection microbiology · 2024Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Influenza A viruses (IAV) can infect a broad range of animal hosts, including humans. In humans, IAV causes seasonal annual epidemics and occasional pandemics, representing a serious public health and economic problem, which is most effectively prevented through vaccination. The defense mechanisms that the host innate immune system provides restrict IAV replication and infection. Consequently, to successfully replicate in interferon (IFN)-competent systems, IAV has to counteract host antiviral activities, mainly the production of IFN and the activities of IFN-induced host proteins that inhibit virus replication. The IAV multifunctional proteins PA-X and NS1 are virulence factors that modulate the innate immune response and virus pathogenicity. Notably, these two viral proteins have synergistic effects in the inhibition of host protein synthesis in infected cells, although using different mechanisms of action. Moreover, the control of innate immune responses by the IAV NS1 and PA-X proteins is subject to a balance that can determine virus pathogenesis and fitness, and recent evidence shows co-evolution of these proteins in seasonal viruses, indicating that they should be monitored for enhanced virulence. Importantly, inhibition of host gene expression by the influenza NS1 and/or PA-X proteins could be explored to develop improved live-attenuated influenza vaccines (LAIV) by modulating the ability of the virus to counteract antiviral host responses. Likewise, both viral proteins represent a reasonable target for the development of new antivirals for the control of IAV infections. In this review, we summarize the role of IAV NS1 and PA-X in controlling the antiviral response during viral 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.