ArticlePLoS pathogens2018
MERS-CoV 4b protein interferes with the NF-κB-dependent innate immune response during infection.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 124 citations in OpenAlex.
- Article
- Modulation of Host Innate Immune Response by Highly Pathogenic Human Coronaviruses during Viral Infection.Journal of microbiology and biotechnology · 2026Review
- Clade C MERS-CoV camel strains vary in protease utilization during viral entry.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- MERS-CoV accessory ORF proteins in innate immune evasion: an evidence-graded functional framework.Frontiers in immunology · 2026Review
- Viral interference of nucleocytoplasmic transport.The Journal of biological chemistry · 2025Review
- Heterologous expression of HCoV-HKU1 ORF 7b by mouse hepatitis virus protects against severe disease during murine infection.PLoS pathogens · 2025Article
- Clade C MERS-CoV camel strains vary in protease utilization during viral entry.bioRxiv : the preprint server for biology · 2025Article
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
- Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025Review
- Tuning the tropism and infectivity of SARS-CoV-2 virus-like particles for mRNA delivery.Nucleic acids research · 2025Article
- Review
- 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
- Review
- SARS-CoV-2 Nsp8 suppresses MDA5 antiviral immune responses by impairing TRIM4-mediated K63-linked polyubiquitination.PLoS pathogens · 2023Article
- Noncanonical Rab9a action supports retromer-mediated endosomal exit of human papillomavirus during virus entry.PLoS pathogens · 2023Article
- Contribution to pathogenesis of accessory proteins of deadly human coronaviruses.Frontiers in cellular and infection microbiology · 2023Review
- Clinical and prognostic significance of long non-coding RNA CRNDE expression in severe pneumonia and its correlation with inflammatory factor levels.American journal of translational research · 2023Article
- UBR5 Acts as an Antiviral Host Factor against MERS-CoV via Promoting Ubiquitination and Degradation of ORF4b.Journal of virology · 2022Article
- Evaluation of alpaca tracheal explants as an ex vivo model for the study of Middle East respiratory syndrome coronavirus (MERS-CoV) infection.Veterinary research · 2022Article
- MERS-CoV ORF4b is a virulence factor involved in the inflammatory pathology induced in the lungs of mice.PLoS pathogens · 2022Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) is a novel human coronavirus that emerged in 2012, causing severe pneumonia and acute respiratory distress syndrome (ARDS), with a case fatality rate of ~36%. When expressed in isolation, CoV accessory proteins have been shown to interfere with innate antiviral signaling pathways. However, there is limited information on the specific contribution of MERS-CoV accessory protein 4b to the repression of the innate antiviral response in the context of infection. We found that MERS-CoV 4b was required to prevent a robust NF-κB dependent response during infection. In wild-type virus infected cells, 4b localized to the nucleus, while NF-κB was retained in the cytoplasm. In contrast, in the absence of 4b or in the presence of cytoplasmic 4b mutants lacking a nuclear localization signal (NLS), NF-κB was translocated to the nucleus leading to the expression of pro-inflammatory cytokines. This indicates that NF-κB repression required the nuclear import of 4b mediated by a specific NLS. Interestingly, we also found that both in isolation and during infection, 4b interacted with α-karyopherin proteins in an NLS-dependent manner. In particular, 4b had a strong preference for binding karyopherin-α4 (KPNA4), which is known to translocate the NF-κB protein complex into the nucleus. Binding of 4b to KPNA4 during infection inhibited its interaction with NF-κB-p65 subunit. Thereby we propose a model where 4b outcompetes NF-κB for KPNA4 binding and translocation into the nucleus as a mechanism of interference with the NF-κB-mediated innate immune response.
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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.