ArticleJournal of virology2020
GBP5 Is an Interferon-Induced Inhibitor of Respiratory Syncytial Virus.
Article in Journal of virology, 2020. 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, 51 citations in OpenAlex.
- Article
- Intravenous Immunoglobulin Reveals a Novel Protective Mechanism: Targeting the GBP5-Driven Pyroptosis Axis in Experimental Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Reactive oxygen species promotion drives auranofin's antiviral activity against hepatitis E virus.Journal of virology · 2026Article
- Article
- Bighorn sheep T2T genome assembly reveals differences in immune genes: a potential cause of high morbidity due to respiratory pathogens.bioRxiv : the preprint server for biology · 2025Article
- Review
- Single cell sequencing analysis of respiratory syncytial virus-infected pediatric and adult human nose organoids reveals age differences, proliferative diversity and identifies novel cellular tropism.The Journal of infection · 2025Article
- Guanylate-binding protein 5: a promising biomarker and therapeutic target.Infection and immunity · 2025Review
- Integrative analysis of transcriptome and metabolome profiles reveals immune-metabolic alterations in pulmonary sarcoidosis.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Guanylate binding proteins (GBPs) as novel therapeutic targets against single-stranded RNA viruses.Molecular biology reports · 2025Review
- Role of guanylate-binding protein 5 in inflammatory diseases, immune diseases, cancers, and its potential therapeutic implications.Inflammopharmacology · 2025Review
- Clinical significance and pathogenesis of GBP5 in infectious mononucleosis associated liver injury.Italian journal of pediatrics · 2025Article
- STAT1 mediates the pro-inflammatory role of GBP5 in colitis.Communications biology · 2025Article
- KRT9 is required for GBP5 suppression of human respiratory syncytial virus.Journal of virology · 2025Article
- Decoding microbial carcinogenic strategies: ubiquitination and SUMO modification.Frontiers in microbiology · 2025Review
- Antiviral roles of eosinophils in asthma and respiratory viral infection.Frontiers in allergy · 2025Review
- Article
- Antagonism of BST2/Tetherin, a new restriction factor of respiratory syncytial virus, requires the viral NS1 protein.PLoS pathogens · 2024Article
- The Furin Protease Dependence and Antiviral GBP2 Sensitivity of Murine Leukemia Virus Infection Are Determined by the Amino Acid Sequence at the Envelope Glycoprotein Cleavage Site.International journal of molecular sciences · 2024Article
- The pseudogene GBP1P1 suppresses influenza A virus replication by acting as a protein decoy for DHX9.Journal of virology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Guanylate binding protein 5 (GBP5) belongs to the GTPase subfamily, which is mainly induced by interferon gamma (IFN-γ) and is involved in many important cellular processes, including inflammasome activation and innate immunity against a wide variety of microbial pathogens. However, it is unknown whether GBP5 inhibits respiratory syncytial virus (RSV) infection. In this study, we identified GBP5 as an effector of the anti-RSV activity of IFN-γ and found that in children, the weaker immune response, especially the weaker IFN-γ response and the decreased GBP5 expression, leads to RSV susceptibility. Furthermore, we revealed that GBP5 reduced the cell-associated levels of the RSV small hydrophobic (SH) protein, which was identified as a viroporin. In contrast, overexpression of the SH protein rescued RSV replication in the presence of GBP5. The GBP5-induced decrease in intracellular SH protein levels is because GBP5 promotes the release of the SH protein into the cell culture. Moreover, the GBP5 C583A mutants with changes at the C terminus or the GBP5 ΔC mutant lacking the C-terminal region, which impairs GBP5 localization in the Golgi, could not inhibit RSV infection, whereas the GTPase-defective GBP5 maintained RSV inhibition, suggesting that Golgi localization but not the GTPase activity of GBP5 is required for RSV inhibition. Interestingly, we found that RSV infection or RSV G protein downregulates GBP5 expression by upregulating DZIP3, an E3 ligase, which induces GBP5 degradation through the K48 ubiquitination and proteasomal pathways. Thus, this study reveals a complicated interplay between host restrictive factor GBP5 and RSV infection and provides important information for understanding the pathogenesis of RSV.
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