ArticleiScience2024
Influenza A virus propagation requires the activation of the unfolded protein response and the accumulation of insoluble protein aggregates.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- Early cell-autonomous and niche-mediated epithelial response to influenza infection in primary alveolar organoids.JCI insight · 2026Article
- MAVS oligomerization drives a faster and more efficient antiviral signaling activation at peroxisomes compared to mitochondria.The FEBS journal · 2026Article
- Secondary analysis of influenza a virus-infected cells at single-cell resolution reveals host BANF1 response to individual and combinations of detected segments.Virology journal · 2026Article
- Cell-cell fusion limits activation of the unfolded protein response induced by the Nipah virus glycoproteins.Journal of virology · 2026Article
- RACK1 in host immune response to infections: molecular mechanisms and therapeutic potentials.Frontiers in immunology · 2026Review
- 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
- Early cell autonomous and niche-mediated alveolar epithelial response to influenza infection in primary lung organoids.bioRxiv : the preprint server for biology · 2025Article
- Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection.International journal of molecular sciences · 2025Review
- Alzheimer's disease and infectious agents: a comprehensive review of pathogenic mechanisms and microRNA roles.Frontiers in neuroscience · 2024Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) employs multiple strategies to manipulate cellular mechanisms and support proper virion formation and propagation. In this study, we performed a detailed analysis of the interplay between IAV and the host cells' proteostasis throughout the entire infectious cycle. We reveal that IAV infection activates the inositol requiring enzyme 1 (IRE1) branch of the unfolded protein response, and that this activation is important for an efficient infection. We further observed the accumulation of virus-induced insoluble protein aggregates, containing both viral and host proteins, associated with a dysregulation of the host cell RNA metabolism. Our data indicate that this accumulation is important for IAV propagation and favors the final steps of the infection cycle, more specifically the virion assembly. These findings reveal additional mechanisms by which IAV disrupts host proteostasis and uncovers new cellular targets that can be explored for the development of host-directed antiviral strategies.
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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.