ArticleJournal of virology2018
Genotype 2 Strains of Porcine Reproductive and Respiratory Syndrome Virus Dysregulate Alveolar Macrophage Cytokine Production via the Unfolded Protein Response.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- The host protein SSR4 mediates PRRSV-induced endoplasmic reticulum stress via interaction with Nsp2.Journal of virology · 2026Article
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- EGCG Restricts PRRSV Proliferation by Disturbing Lipid Metabolism.Microbiology spectrum · 2022Article
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- Evaluation of the Impact of Antimicrobial Use Protocols in Porcine Reproductive and Respiratory Syndrome Virus-Infected Swine on Phenotypic Antimicrobial Resistance Patterns.Applied and environmental microbiology · 2022Article
- Critical Roles of G3BP1 in Red-Spotted Grouper Nervous Necrosis Virus-Induced Stress Granule Formation and Viral Replication in Orange-Spotted Grouper (Frontiers in immunology · 2022Article
- Swine Dendritic Cell Response to Porcine Reproductive and Respiratory Syndrome Virus: An Update.Frontiers in immunology · 2021Review
- A porcine macrophage cell line that supports high levels of replication of OURT88/3, an attenuated strain of African swine fever virus.Emerging microbes & infections · 2020Article
- The integrated stress response in pulmonary disease.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection.Virus research · 2020Review
- The role of host eIF2α in viral infection.Virology journal · 2020Review
- Luminespib counteracts the Kifunensine-induced lung endothelial barrier dysfunction.Current research in toxicology · 2020Article
- Effects of Heat Shock Protein 90 Inhibition In the Lungs.Medicine in drug discovery · 2020Article
- Distinctive Cellular and Metabolic Reprogramming in Porcine Lung Mononuclear Phagocytes Infected With Type 1 PRRSV Strains.Frontiers in immunology · 2020Article
- Unfolded Protein Response in Lung Health and Disease.Frontiers in medicine · 2020Article
- Reprogramming the unfolded protein response for replication by porcine reproductive and respiratory syndrome virus.PLoS pathogens · 2019Article
- Signaling pathways involved in regulating apoptosis induction in host cells upon PRRSV infection.Virus genes · 2019Review
- Interaction of PIAS1 with PRRS virus nucleocapsid protein mediates NF-κB activation and triggers proinflammatory mediators during viral infection.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) infects alveolar macrophages (AMϕ), causing dysregulated alpha interferon (IFN-α) and tumor necrosis factor alpha (TNF-α) production through a mechanism(s) yet to be resolved. Here, we show that AMϕ infected with PRRSV secreted a reduced quantity of IFN-α following exposure of the cell to synthetic double-stranded RNA (dsRNA). This reduction did not correlate with reduced IFNA1 gene transcription. Rather, it coincided with two events that occurred late during infection and that were indicative of translational attenuation, specifically, the activation of eukaryotic translation initiation factor 2α (eIF2α) and the appearance of stress granules. Notably, the typical rapid production of TNF-α by AMϕ exposed to lipopolysaccharide (LPS) was suppressed or enhanced by PRRSV, depending on when the LPS exposure occurred after virus infection. If exposure was delayed until 6 h postinfection (hpi) so that the development of the cytokine response coincided with the time in which phosphorylation of eIF2α by the stress sensor PERK (protein kinase RNA [PKR]-like ER kinase) occurred, inhibition of TNF-α production was observed. However, if LPS exposure occurred at 2 hpi, prior to a detectable onset of eIF2α phosphorylation, a synergistic response was observed due to the earlier NF-κB activation via the stress sensor IRE1α (inositol-requiring kinase 1α). These results suggest that the asynchronous actions of two branches of the unfolded protein response (UPR), namely, IRE1α, and PERK, activated by ER stress resulting from the virus infection, are associated with enhancement or suppression of TNF-α production, respectively.
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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.