ArticlemBio2023
Porcine Epidemic Diarrhea Virus Antagonizes Host IFN-λ-Mediated Responses by Tilting Transcription Factor STAT1 toward Acetylation over Phosphorylation To Block Its Activation.
Article in mBio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- PRMT3 restricts porcine epidemic diarrhea virus replication by disrupting the interaction between VAPA and the viral nucleocapsid protein.PLoS pathogens · 2026Article
- The Interplay Between Autophagy and Porcine Epidemic Diarrhea Virus: From Molecular Mechanisms to Therapeutic Perspectives.Microorganisms · 2026Review
- Cyclo-C stabilizes PEX13 to inhibit porcine epidemic diarrhea virus replication by blocking pexophagy-mediated disruption of antiviral innate immunity.Journal of virology · 2026Article
- The Compound Terminalia Chebula Extract Alleviates PEDV-Induced Colonic Injury in Suckling Piglets by Enhancing Antioxidant Capacity, Suppressing Inflammation, Restoring Intestinal Function, and Inhibiting Viral Replication.Animals : an open access journal from MDPI · 2026Article
- PDK4-driven lactate accumulation facilitates LPCAT2 lactylation to exacerbate sepsis-induced acute lung injury.Cell death and differentiation · 2026Article
- PEDV Structural Proteins with Emphasis on M Protein as an Immunomodulatory Factor in Porcine Innate Immunity.Life (Basel, Switzerland) · 2025Review
- Article
- The function and mechanism of protein acylation in the regulation of viral infection.Virulence · 2025Review
- Nuclear shuttling of CDC4 mediated broad-spectrum antiviral activity against diverse coronaviruses.Emerging microbes & infections · 2025Article
- How Does Porcine Epidemic Diarrhea Virus Escape Host Innate Immunity?Pathogens (Basel, Switzerland) · 2025Review
- Dose-Dependent Porcine Deltacoronavirus Infection Reveals Linkage Between Infectious Dose and Immune Response.Animals : an open access journal from MDPI · 2025Article
- Article
- Article
- Coronavirus nucleocapsid proteins: a multifaceted modulator in the innate immune evasion.Frontiers in microbiology · 2025Review
- Integrating network pharmacology with pharmacological research to elucidate the mechanism of modified Gegen Qinlian Decoction in treating porcine epidemic diarrhea.Scientific reports · 2024Article
- Developing Next-Generation Live Attenuated Vaccines for Porcine Epidemic Diarrhea Using Reverse Genetic Techniques.Vaccines · 2024Review
- Review
- Mechanisms of mesothelial cell response to viral infections: HDAC1-3 inhibition blocks poly(I:C)-induced type I interferon response and modulates the mesenchymal/inflammatory phenotype.Frontiers in cellular and infection microbiology · 2024Article
- Broad antagonism of coronaviruses nsp5 to evade the host antiviral responses by cleaving POLDIP3.PLoS pathogens · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine epidemic diarrhea virus (PEDV) is the main etiologic agent causing acute swine epidemic diarrhea, leading to severe economic losses to the pig industry. PEDV has evolved to deploy complicated antagonistic strategies to escape from host antiviral innate immunity. Our previous study demonstrated that PEDV downregulates histone deacetylase 1 (HDAC1) expression by binding viral nucleocapsid (N) protein to the transcription factor Sp1, inducing enhanced protein acetylation. We hypothesized that PEDV inhibition of HDAC1 expression would enhance acetylation of the molecules critical in innate immune signaling. Signal transducer and activator of transcription 1 (STAT1) is a crucial transcription factor regulating expression of interferon (IFN)-stimulated genes (ISGs) and anti-PEDV immune responses, as shown by overexpression, chemical inhibition, and gene knockdown in IPEC-J2 cells. We further show that PEDV infection and its N protein overexpression, although they upregulated STAT1 transcription level, could significantly block poly(I·C) and IFN-λ3-induced STAT1 phosphorylation and nuclear localization. Western blotting revealed that PEDV and its N protein promote STAT1 acetylation via downregulation of HDAC1. Enhanced STAT1 acetylation due to HDAC1 inhibition by PEDV or MS-275 (an HDAC1 inhibitor) impaired STAT1 phosphorylation, indicating that STAT1 acetylation negatively regulated its activation. These results, together with our recent report on PEDV N-mediated inhibition of Sp1, clearly indicate that PEDV manipulates the Sp1-HDAC1-STAT1 signaling axis to inhibit transcription of
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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.