ArticleVirology2018
Accessory proteins 8b and 8ab of severe acute respiratory syndrome coronavirus suppress the interferon signaling pathway by mediating ubiquitin-dependent rapid degradation of interferon regulatory factor 3.
Article in Virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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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
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Spatial Transcriptomics and Single Cell-RNASeq Reveals Cellular Heterogeneity of SARS-CoV-2 in Lung Tissues and Global Mutational Patterns in COVID-19 Patients.Journal of medical virology · 2025Article
- MDA5 Is a Major Determinant of Developing Symptoms in Critically Ill COVID-19 Patients.Clinical reviews in allergy & immunology · 2024Review
- Viral strategies to antagonize the host antiviral innate immunity: an indispensable research direction for emerging virus-host interactions.Emerging microbes & infections · 2024Review
- Chaperone- and PTM-mediated activation of IRF1 tames radiation-induced cell death and the inflammatory response.Cellular & molecular immunology · 2024Article
- Multiple E3 ligases act as antiviral factors against SARS-CoV-2 via inducing the ubiquitination and degradation of ORF9b.Journal of virology · 2024Article
- SARS-CoV-2 ORF8 modulates lung inflammation and clinical disease progression.PLoS pathogens · 2024Article
- Aggregated Hendra virus C-protein activates the NLRP3 inflammasome to induce inflammation.Journal of inflammation (London, England) · 2023Article
- Possible Pathogenesis and Prevention of Long COVID: SARS-CoV-2-Induced Mitochondrial Disorder.International journal of molecular sciences · 2023Review
- Review
- L-shaped distribution of the relative substitution rate (c/μ) observed for SARS-COV-2's genome, inconsistent with the selectionist theory, the neutral theory and the nearly neutral theory but a near-neutral balanced selection theory: Implication on "neutralist-selectionist" debate.Computers in biology and medicine · 2023Article
- Contribution to pathogenesis of accessory proteins of deadly human coronaviruses.Frontiers in cellular and infection microbiology · 2023Review
- Ubiquitination of SARS-CoV-2 ORF7a Prevents Cell Death Induced by Recruiting BclXL To Activate ER Stress.Microbiology spectrum · 2022Article
- Plant Molecular Pharming and Plant-Derived Compounds towards Generation of Vaccines and Therapeutics against Coronaviruses.Vaccines · 2022Review
- The First Geographic Identification by Country of Sustainable Mutations of SARS-COV2 Sequence Samples: Worldwide Natural Selection Trends.bioRxiv : the preprint server for biology · 2022Article
- Host-Genome Similarity Characterizes the Adaption of SARS-CoV-2 to Humans.Biomolecules · 2022Article
- Myeloid-derived suppressor cells in COVID-19: A review.Clinical immunology (Orlando, Fla.) · 2022Review
- Inflammasome regulation in driving COVID-19 severity in humans and immune tolerance in bats.Journal of leukocyte biology · 2022Review
- Structural biology of SARS-CoV-2: open the door for novel therapies.Signal transduction and targeted therapy · 2022Review
- Covid-19: virology, variants, and vaccines.BMJ medicine · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) is an inefficient inducer of interferon (IFN) response. It expresses various proteins that effectively circumvent IFN production at different levels via distinct mechanisms. Through the construction of recombinant IBV expressing proteins 8a, 8b and 8ab encoded by SARS-CoV ORF8, we demonstrate that expression of 8b and 8ab enables the corresponding recombinant viruses to partially overcome the inhibitory actions of IFN activation to achieve higher replication efficiencies in cells. We also found that proteins 8b and 8ab could physically interact with IRF3. Overexpression of 8b and 8ab resulted in the reduction of poly (I:C)-induced IRF3 dimerization and inhibition of the IFN-β signaling pathway. This counteracting effect was partially mediated by protein 8b/8ab-induced degradation of IRF3 in a ubiquitin-proteasome-dependent manner. Taken together, we propose that SARS-CoV may exploit the unique functions of proteins 8b and 8ab as novel mechanisms to overcome the effect of IFN response during virus infection.
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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.