ArticlePLoS pathogens2009
P58(IPK): a novel "CIHD" member of the host innate defense response against pathogenic virus infection.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- A chemokine gene expression signature derived from meta-analysis predicts the pathogenicity of viral respiratory infections.BMC systems biology · 2011Pooled it
- Insulin-mediated endothelin signaling is antiviral during West Nile virus infection.bioRxiv : the preprint server for biology · 2023Article
- Hantaviruses use the endogenous host factor P58IPK to combat the PKR antiviral response.PLoS pathogens · 2021Article
- The Role of Nucleic Acid Sensing in Controlling Microbial and Autoimmune Disorders.International review of cell and molecular biology · 2019Review
- Analysis of Drosophila STING Reveals an Evolutionarily Conserved Antimicrobial Function.Cell reports · 2018Article
- Nucleic acid sensing and innate immunity: signaling pathways controlling viral pathogenesis and autoimmunity.Current clinical microbiology reports · 2016Article
- p58(IPK) suppresses NLRP3 inflammasome activation and IL-1β production via inhibition of PKR in macrophages.Scientific reports · 2016Article
- Robust expression of vault RNAs induced by influenza A virus plays a critical role in suppression of PKR-mediated innate immunity.Nucleic acids research · 2015Article
- Role of p58IPK in Endoplasmic Reticulum Stress-associated Apoptosis and Inflammation.Journal of ophthalmic & vision research · 2014Article
- Deletion of P58(IPK), the Cellular Inhibitor of the Protein Kinases PKR and PERK, Causes Bone Changes and Joint Degeneration in Mice.Frontiers in endocrinology · 2014Article
- Influenza virus-induced lung inflammation was modulated by cigarette smoke exposure in mice.PloS one · 2014Article
- Host-directed therapeutics for tuberculosis: can we harness the host?Microbiology and molecular biology reviews : MMBR · 2013Review
- Systems approaches to influenza-virus host interactions and the pathogenesis of highly virulent and pandemic viruses.Seminars in immunology · 2013Review
- Tinkering with translation: protein synthesis in virus-infected cells.Cold Spring Harbor perspectives in biology · 2013Review
- Improved control of tuberculosis and activation of macrophages in mice lacking protein kinase R.PloS one · 2012Article
- Mannose-binding lectin contributes to deleterious inflammatory response in pandemic H1N1 and avian H9N2 infection.The Journal of infectious diseases · 2012Article
- Viral subversion of the host protein synthesis machinery.Nature reviews. Microbiology · 2011Review
- Virus infection rapidly activates the P58(IPK) pathway, delaying peak kinase activation to enhance viral replication.Virology · 2011Article
- Coronavirus gene 7 counteracts host defenses and modulates virus virulence.PLoS pathogens · 2011Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
To support their replication, viruses take advantage of numerous cellular factors and processes. Recent large-scale screens have identified hundreds of such factors, yet little is known about how viruses exploit any of these. Influenza virus infection post-translationally activates P58(IPK), a cellular inhibitor of the interferon-induced, dsRNA-activated eIF2alpha kinase, PKR. Here, we report that infection of P58(IPK) knockout mice with influenza virus resulted in increased lung pathology, immune cell apoptosis, PKR activation, and mortality. Analysis of lung transcriptional profiles, including those induced by the reconstructed 1918 pandemic virus, revealed increased expression of genes associated with the cell death, immune, and inflammatory responses. These experiments represent the first use of a mammalian infection model to demonstrate the role of P58(IPK) in the antiviral response. Our results suggest that P58(IPK) represents a new class of molecule, a cellular inhibitor of the host defense (CIHD), as P58(IPK) is activated during virus infection to inhibit virus-induced apoptosis and inflammation to prolong host survival, even while prolonging viral replication.
Indexed as
Identifiers
What OpenQuestion holds
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.