ArticleJournal of virology2015
Infectious Bronchitis Coronavirus Inhibits STAT1 Signaling and Requires Accessory Proteins for Resistance to Type I Interferon Activity.
Article in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Coronavirus endoribonuclease nsp15 suppresses host protein synthesis and evades PKR-eIF2α-mediated translation shutoff to ensure viral protein synthesis.PLoS pathogens · 2025Article
- The long non-coding RNA lncRNA-DRNR enhances infectious bronchitis virus replication by targeting chicken JMJD6 and modulating interferon-stimulated genes expression via the JAK-STAT signalling pathway.Veterinary research · 2024Article
- Coronavirus nucleocapsid protein enhances the binding of p-PKCα to RACK1: Implications for inhibition of nucleocytoplasmic trafficking and suppression of the innate immune response.PLoS pathogens · 2024Article
- Potential Transcriptional Enhancers in Coronaviruses: From Infectious Bronchitis Virus to SARS-CoV-2.International journal of molecular sciences · 2024Article
- Deciphering infected cell types, hub gene networks and cell-cell communication in infectious bronchitis virus via single-cell RNA sequencing.PLoS pathogens · 2024Article
- The role of IBV PL1pro in virus replication and suppression of host innate immune responses.BMC veterinary research · 2023Article
- Global Emergence of Infectious Bronchitis Virus Variants: Evolution, Immunity, and Vaccination Challenges.Transboundary and emerging diseases · 2023Review
- Infectious Bronchitis Virus Nsp14 Degrades JAK1 to Inhibit the JAK-STAT Signaling Pathway in HD11 Cells.Viruses · 2022Article
- Article
- Current Knowledge on Infectious Bronchitis Virus Non-structural Proteins: The Bearer for Achieving Immune Evasion Function.Frontiers in veterinary science · 2022Review
- Interplay of the ubiquitin proteasome system and the innate immune response is essential for the replication of infectious bronchitis virus.Archives of virology · 2021Article
- Review
- Identification and analysis of long non-coding RNAs and mRNAs in chicken macrophages infected with avian infectious bronchitis coronavirus.BMC genomics · 2021Article
- The Interplay Between Coronavirus and Type I IFN Response.Frontiers in microbiology · 2021Review
- Emerging infectious bronchitis virus (IBV) in Egypt: Evidence for an evolutionary advantage of a new S1 variant with a unique gene 3ab constellation.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020Article
- Candesartan could ameliorate the COVID-19 cytokine storm.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020Article
- Infectious Bronchitis Coronavirus Infection in Chickens: Multiple System Disease with Immune Suppression.Pathogens (Basel, Switzerland) · 2020Review
- The Characterization ofGenes · 2020Article
- Antiviral responses against chicken respiratory infections: Focus on avian influenza virus and infectious bronchitis virus.Cytokine · 2020Review
- COVID-19 Outbreak: Pathogenesis, Current Therapies, and Potentials for Future Management.Frontiers in pharmacology · 2020Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
unlabelledThe innate immune response is the first line of defense against viruses, and type I interferon (IFN) is a critical component of this response. Similar to other viruses, the gammacoronavirus infectious bronchitis virus (IBV) has evolved under evolutionary pressure to evade and counteract the IFN response to enable its survival. Previously, we reported that IBV induces a delayed activation of the IFN response. In the present work, we describe the resistance of IBV to IFN and the potential role of accessory proteins herein. We show that IBV is fairly resistant to the antiviral state induced by IFN and identify that viral accessory protein 3a is involved in resistance to IFN, as its absence renders IBV less resistant to IFN treatment. In addition to this, we found that independently of its accessory proteins, IBV inhibits IFN-mediated phosphorylation and translocation of STAT1. In summary, we show that IBV uses multiple strategies to counteract the IFN response. IMPORTANCE: In the present study, we show that infectious bronchitis virus (IBV) is resistant to IFN treatment and identify a role for accessory protein 3a in the resistance against the type I IFN response. We also demonstrate that, in a time-dependent manner, IBV effectively interferes with IFN signaling and that its accessory proteins are dispensable for this activity. This study demonstrates that the gammacoronavirus IBV, similar to its mammalian counterparts, has evolved multiple strategies to efficiently counteract the IFN response of its avian host, and it identifies accessory protein 3a as multifaceted antagonist of the avian IFN system.
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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.