ArticleCell reports2015
Acute Lung Injury Results from Innate Sensing of Viruses by an ER Stress Pathway.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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
33 citing papers in PubMed, 61 citations in OpenAlex.
- RNF5 promotes acute lung injury through HSPA5 ER-to-cytosol translocation and resultant PERK activation.Cell death and differentiation · 2026Article
- Article
- Chronic Lung Allograft Dysfunction: Clinical Manifestations and Immunologic Mechanisms.Transplantation · 2025Review
- SARS-CoV-2 S, M, and E Structural Glycoproteins Differentially Modulate Endoplasmic Reticulum Stress Responses.International journal of molecular sciences · 2025Article
- H5 subtype avian influenza virus induces Golgi apparatus stress response via TFE3 pathway to promote virus replication.PLoS pathogens · 2024Article
- Protein Glycosylation Patterns Shaped By the IRE1-XBP1s Arm of the Unfolded Protein Response.Israel journal of chemistry · 2024Article
- The Hemagglutinin of Influenza A Virus Induces Ferroptosis to Facilitate Viral Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Innate IRE1α-XBP1 activation by viral single-stranded RNA and its influence on lung cytokine production during SARS-CoV-2 pneumonia.Genes and immunity · 2024Article
- Long-term evolution of human seasonal influenza virus A(H3N2) is associated with an increase in polymerase complex activity.Virus evolution · 2024Article
- Microvascular lung injury and endoplasmic reticulum stress in systemic lupus erythematosus-associated alveolar hemorrhage and pulmonary vasculitis.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Alleviation of Endoplasmic Reticulum Stress Enhances Human Corneal Epithelial Cell Viability under Hyperosmotic Conditions.International journal of molecular sciences · 2022Article
- Article
- Influenza A viruses balance ER stress with host protein synthesis shutoff.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Age-Dependent Glycomic Response to the 2009 Pandemic H1N1 Influenza Virus and Its Association with Disease Severity.Journal of proteome research · 2020Article
- Glycomic analysis of host response reveals high mannose as a key mediator of influenza severity.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- NOD1 and NOD2 Activation by Diverse Stimuli: a Possible Role for Sensing Pathogen-Induced Endoplasmic Reticulum Stress.Infection and immunity · 2020Review
- Endoplasmic reticulum stress promotes inflammation-mediated proteolytic activity at the ocular surface.Scientific reports · 2020Article
- Pathological Aspects of COVID-19 as a Conformational Disease and the Use of Pharmacological Chaperones as a Potential Therapeutic Strategy.Frontiers in pharmacology · 2020Review
- The Establishment and Validation of the Human U937 Cell Line as a Cellular Model to Screen Immunomodulatory Agents Regulating Cytokine Release Induced by Influenza Virus Infection.Virologica Sinica · 2019Article
- The Importance of Vaccinating Children and Pregnant Women against Influenza Virus Infection.Pathogens (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Incursions of new pathogenic viruses into humans from animal reservoirs are occurring with alarming frequency. The molecular underpinnings of immune recognition, host responses, and pathogenesis in this setting are poorly understood. We studied pandemic influenza viruses to determine the mechanism by which increasing glycosylation during evolution of surface proteins facilitates diminished pathogenicity in adapted viruses. ER stress during infection with poorly glycosylated pandemic strains activated the unfolded protein response, leading to inflammation, acute lung injury, and mortality. Seasonal strains or viruses engineered to mimic adapted viruses displaying excess glycans on the hemagglutinin did not cause ER stress, allowing preservation of the lungs and survival. We propose that ER stress resulting from recognition of non-adapted viruses is utilized to discriminate "non-self" at the level of protein processing and to activate immune responses, with unintended consequences on pathogenesis. Understanding this mechanism should improve strategies for treating acute lung injury from zoonotic viral infections.
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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.