ArticleJournal of virology2005
Contribution of trafficking signals in the cytoplasmic tail of the infectious bronchitis virus spike protein to virus infection.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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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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
28 citing papers in PubMed, 36 citations in OpenAlex.
- An unconventional HxD motif orchestrates coatomer-dependent coronavirus morphogenesis.bioRxiv : the preprint server for biology · 2025Article
- Adaptive truncation of the S gene in IBV during chicken embryo passaging plays a crucial role in its attenuation.PLoS pathogens · 2024Article
- The N1038S Substitution andFrontiers in microbiology · 2022Article
- Cell Entry of Animal Coronaviruses.Viruses · 2021Review
- A Virulent PEDV Strain FJzz1 with Genomic Mutations and Deletions at the High Passage Level Was Attenuated in Piglets via Serial Passage In Vitro.Virologica Sinica · 2021Article
- Sequences in the cytoplasmic tail of SARS-CoV-2 Spike facilitate expression at the cell surface and syncytia formation.Nature communications · 2021Article
- Fusogenicity of the Ghana Virus (Viruses · 2019Article
- Development of a recombinant Newcastle disease virus-vectored vaccine for infectious bronchitis virus variant strains circulating in Egypt.Veterinary research · 2019Article
- Deletion of both the Tyrosine-Based Endocytosis Signal and the Endoplasmic Reticulum Retrieval Signal in the Cytoplasmic Tail of Spike Protein Attenuates Porcine Epidemic Diarrhea Virus in Pigs.Journal of virology · 2019Article
- Structural insights into coronavirus entry.Advances in virus research · 2019Article
- Article
- Coronavirus S protein-induced fusion is blocked prior to hemifusion by Abl kinase inhibitors.The Journal of general virology · 2018Article
- Characterization of an Immunodominant Epitope in the Endodomain of the Coronavirus Membrane Protein.Viruses · 2016Article
- The contribution of the cytoplasmic retrieval signal of severe acute respiratory syndrome coronavirus to intracellular accumulation of S proteins and incorporation of S protein into virus-like particles.The Journal of general virology · 2016Article
- Altered pathogenicity of a tl/CH/LDT3/03 genotype infectious bronchitis coronavirus due to natural recombination in the 5'- 17kb region of the genome.Virus research · 2016Article
- A Coronavirus E Protein Is Present in Two Distinct Pools with Different Effects on Assembly and the Secretory Pathway.Journal of virology · 2015Article
- Review
- Progress and challenges toward the development of vaccines against avian infectious bronchitis.Journal of immunology research · 2015Review
- Characterization of the spike protein of human coronavirus NL63 in receptor binding and pseudotype virus entry.Virus research · 2011Article
- The hydrophobic domain of infectious bronchitis virus E protein alters the host secretory pathway and is important for release of infectious virus.Journal of virology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Coronavirus spike (S) proteins are responsible for binding and fusion with target cells and thus play an essential role in virus infection. Recently, we identified a dilysine endoplasmic reticulum (ER) retrieval signal and a tyrosine-based endocytosis signal in the cytoplasmic tail of the S protein of infectious bronchitis virus (IBV). Here, an infectious cDNA clone of IBV was used to address the importance of the S protein trafficking signals to virus infection. We constructed infectious cDNA clones lacking the ER retrieval signal, the endocytosis signal, or both. The virus lacking the ER retrieval signal was viable. However, this virus had a growth defect at late times postinfection and produced larger plaques than IBV. Further analysis confirmed that the mutant S protein trafficked though the secretory pathway faster than wild-type S protein. A more dramatic phenotype was obtained when the endocytosis signal was mutated. Recombinant viruses lacking the endocytosis signal (in combination with a mutated dilysine signal or alone) could not be recovered, even though transient syncytia were formed in transfected cells. Our results suggest that the endocytosis signal of IBV S is essential for productive 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.