ArticlePLoS pathogens2018
Specificity and functional interplay between influenza virus PA-X and NS1 shutoff activity.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 51 citations in OpenAlex.
- Divergent pathogenic mechanisms of influenza A and influenza B viruses.Archives of microbiology · 2026Review
- N-terminal acetylation controls multiple functional aspects of the influenza A virus ribonuclease PA-X.Journal of virology · 2026Article
- Enhanced genome replication activity of pandemic H1N1 influenza A virus through PA mutations.Journal of virology · 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 ribosomal landscape in influenza A virus infection: from molecular mechanisms to clinical relevance.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Molecular arms races at the virus-host splicing interface and their pathogenic implications.Frontiers in microbiology · 2026Review
- 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
- N-terminal acetylation controls multiple functional aspects of the influenza A virus ribonuclease PA-X.bioRxiv : the preprint server for biology · 2025Article
- Seasonal influenza a virus lineages exhibit divergent abilities to antagonize interferon induction and signaling.PLoS pathogens · 2024Article
- Functional Analysis of GRSF1 in the Nuclear Export and Translation of Influenza A Virus mRNAs.Viruses · 2024Article
- Human coronavirus NL63 nsp1 induces degradation of RNA polymerase II to inhibit host protein synthesis.PLoS pathogens · 2024Article
- Molecular Markers and Mechanisms of Influenza A Virus Cross-Species Transmission and New Host Adaptation.Viruses · 2024Review
- Influenza A virus NS1 effector domain is required for PA-X-mediated host shutoff in infected cells.Journal of virology · 2024Article
- Fitness Determinants of Influenza A Viruses.Viruses · 2023Review
- Influenza A virus inhibits TET2 expression by endoribonuclease PA-X to attenuate type I interferon signaling and promote viral replication.PLoS pathogens · 2023Article
- Cut site preference allows influenza A virus PA-X to discriminate between host and viral mRNAs.Nature microbiology · 2023Article
- NS1 and PA-X of H1N1/09 influenza virus act in a concerted manner to manipulate the innate immune response of porcine respiratory epithelial cells.Frontiers in cellular and infection microbiology · 2023Article
- Strategies of Influenza A Virus to Ensure the Translation of Viral mRNAs.Pathogens (Basel, Switzerland) · 2022Review
- Exosomes Released by Influenza-Virus-Infected Cells Carry Factors Capable of Suppressing Immune Defense Genes in Naïve Cells.Viruses · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Influenza A viruses modulate host antiviral responses to promote viral growth and pathogenicity. Through viral PA-X and NS1 proteins, the virus is capable of suppressing host protein synthesis, termed "host shutoff." Although both proteins are known to induce general shutoff, specificity of target genes and their functional interplay in mediating host shutoff are not fully elucidated. In this study, we generated four recombinant influenza A/California/04/2009 (pH1N1) viruses containing mutations affecting the expression of active PA-X and NS1. We analyzed viral growth, general shutoff activity, specificity of mRNA targets, and viral gene expressions. Our results showed that PA-X was the major contributor in reducing general host protein expression in the virus-infected cells. Intriguingly, our transcriptomic analysis from infected human airway A549 cells indicate that shutoff-active NS1 specifically targeted host mRNAs related to interferon (IFN) signaling pathways and cytokine release. Specificity of target mRNAs was less evident in PA-X, although it preferentially degraded genes associated with cellular protein metabolism and protein repair. Interestingly, in the presence of shutoff-active NS1, PA-X also degraded viral mRNAs, especially NS segments. The virus expressing shutoff-active NS1 with reduced amount of PA-X expression most efficiently suppressed antiviral and innate immune responses in human cells, indicating that influenza virus needs to optimize the contribution of these two shutoff proteins to circumvent host responses for its optimum growth.
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