ArticleProceedings of the National Academy of Sciences of the United States of America2021
Influenza A viruses balance ER stress with host protein synthesis shutoff.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- GRP78 dysregulation: A proposed molecular mechanism linking the tumor microenvironment to sepsis susceptibility in patients with cancer (Review).International journal of molecular medicine · 2026Review
- GRP78 in viral pneumonia: dual regulatory mechanisms and translational prospects.Clinical and experimental medicine · 2026Review
- Degradation of ACSL3 by influenza A virus shifts unfolded protein response from antiviral defense to viral evasion.Virologica Sinica · 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
- Influenza A virus induces PI4P production at the endoplasmic reticulum in an ATG16L1-dependent manner to promote the egress of viral ribonucleoproteins.PLoS biology · 2025Article
- An atlas of protein phosphorylation dynamics during interferon signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Autophagy and Respiratory Viruses: Mechanisms, Viral Exploitation, and Therapeutic Insights.Cells · 2025Review
- Review
- Dietary phosphorus restriction induced phospholipid deficiency, endoplasmic reticulum stress, inflammatory response and gut microbiota disorders inFrontiers in immunology · 2025Article
- H5 subtype avian influenza virus induces Golgi apparatus stress response via TFE3 pathway to promote virus replication.PLoS pathogens · 2024Article
- Viral strategies to antagonize the host antiviral innate immunity: an indispensable research direction for emerging virus-host interactions.Emerging microbes & infections · 2024Review
- Modulation of diverse biological processes by CPSF, the master regulator of mRNA 3' ends.RNA (New York, N.Y.) · 2024Review
- Article
- Infectious bursal disease virus VP5 triggers host shutoff in a transcription-dependent manner.mBio · 2024Article
- The ER-Golgi transport of influenza virus through NS1-Sec13 association during virus replication.Microbiology spectrum · 2024Article
- Insight into Antiviral Activity of Ag/TiOInternational journal of nanomedicine · 2024Article
- The cGAS-STING pathway in viral infections: a promising link between inflammation, oxidative stress and autophagy.Frontiers in immunology · 2024Review
- ATG9A regulates the dissociation of recycling endosomes from microtubules to form liquid influenza A virus inclusions.PLoS biology · 2023Article
- Modulation of Influenza A virus NS1 expression reveals prioritization of host response antagonism at single-cell resolution.Frontiers in microbiology · 2023Article
- Strategies of Influenza A Virus to Ensure the Translation of Viral mRNAs.Pathogens (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Excessive production of viral glycoproteins during infections poses a tremendous stress potential on the endoplasmic reticulum (ER) protein folding machinery of the host cell. The host cell balances this by providing more ER resident chaperones and reducing translation. For viruses, this unfolded protein response (UPR) offers the potential to fold more glycoproteins. We postulated that viruses could have developed means to limit the inevitable ER stress to a beneficial level for viral replication. Using a relevant human pathogen, influenza A virus (IAV), we first established the determinant for ER stress and UPR induction during infection. In contrast to a panel of previous reports, we identified neuraminidase to be the determinant for ER stress induction, and not hemagglutinin. IAV relieves ER stress by expression of its nonstructural protein 1 (NS1). NS1 interferes with the host messenger RNA processing factor CPSF30 and suppresses ER stress response factors, such as XBP1. In vivo viral replication is increased when NS1 antagonizes ER stress induction. Our results reveal how IAV optimizes glycoprotein expression by balancing folding capacity.
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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.