ArticleVirus research2011
Characterization of the spike protein of human coronavirus NL63 in receptor binding and pseudotype virus entry.
Article in Virus research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Receptor binding domain-independent pancoronavirus vaccine design by fusion of conserved T/B Epitopes.Emerging microbes & infections · 2026Article
- Clues to Long COVID Linked to Virulence and Infectivity Found in Shell Proteins.Advances in respiratory medicine · 2026Review
- Genetic characterization of coronaviruses causing common cold symptoms based on micro-targeted capture sequencing.Archives of virology · 2025Article
- Characterization of spike S1/S2 processing and entry pathways of lentiviral pseudoviruses bearing seasonal human coronaviruses NL63, 229E, and HKU1 spikes.Microbiology spectrum · 2025Article
- Rapid Degradation of the Human ACE2 Receptor Upon Binding and Internalization of SARS-Cov-2-Spike-RBD Protein.bioRxiv : the preprint server for biology · 2024Article
- Seasonal human coronavirus NL63 epidemics in children in Guilin, China, reveal the emergence of a new subgenotype of HCoV-NL63.Frontiers in cellular and infection microbiology · 2024Article
- Characterization of CCoV-HuPn-2018 spike protein-mediated viral entry.Journal of virology · 2023Article
- Molecular mechanisms of human coronavirus NL63 infection and replication.Virus research · 2023Review
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- Cell Entry of Animal Coronaviruses.Viruses · 2021Review
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- Comparison of Four SARS-CoV-2 Neutralization Assays.Vaccines · 2020Article
- LY6E Restricts Entry of Human Coronaviruses, Including Currently Pandemic SARS-CoV-2.Journal of virology · 2020Article
- Quantifying absolute neutralization titers against SARS-CoV-2 by a standardized virus neutralization assay allows for cross-cohort comparisons of COVID-19 sera.medRxiv : the preprint server for health sciences · 2020Article
- Discovery of a subgenotype of human coronavirus NL63 associated with severe lower respiratory tract infection in China, 2018.Emerging microbes & infections · 2020Article
- Membrane Protein of Human Coronavirus NL63 Is Responsible for Interaction with the Adhesion Receptor.Journal of virology · 2019Article
- Human Coronavirus NL63 Molecular Epidemiology and Evolutionary Patterns in Rural Coastal Kenya.The Journal of infectious diseases · 2018Article
- Identification of Residues Controlling Restriction versus Enhancing Activities of IFITM Proteins on Entry of Human Coronaviruses.Journal of virology · 2018Article
- Inhibition of endoplasmic reticulum-resident glucosidases impairs severe acute respiratory syndrome coronavirus and human coronavirus NL63 spike protein-mediated entry by altering the glycan processing of angiotensin I-converting enzyme 2.Antimicrobial agents and chemotherapy · 2015Article
- Human coronaviruses: Clinical features and phylogenetic analysis.BioMedicine · 2013Review
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8 authors.
Funding
Abstract
The spike (S) protein of human coronavirus NL63 (HCoV-NL63) mediates both cell attachment by binding to its receptor hACE2 and membrane fusion during virus entry. We have previously identified the receptor-binding domain (RBD) and residues important for RBD-hACE2 association. Here, we further characterized the S protein by investigating the roles of the cytoplasmic tail and 19 residues located in the RBD in protein accumulation, receptor binding, and pseudotype virus entry. For these purposes, we first identified an entry-efficient S gene template from a pool of gene variants and used it as a backbone to generate a series of cytoplasmic tail deletion and single residue substitution mutants. Our results showed that: (i) deletion of 18aa from the C-terminus enhanced the S protein accumulation and virus entry, which might be due to the deletion of intracellular retention signals; (ii) further deletion to residue 29 also enhanced the amount of S protein on the cell surface and in virion, but reduced virus entry by 25%, suggesting that residues 19-29 contributes to membrane fusion; (iii) a 29aa-deletion mutant had a defect in anchoring on the plasma membrane, which led to a dramatic decrease of S protein in virion and virus entry; (iv) a total of 15 residues (Y498, V499, V531, G534, G537, D538, S540, G575, S576, E582, W585, Y590, T591, V593 and G594) within RBD were important for receptor binding and virus entry. They probably form three receptor binding motifs, and the third motif is conserved between NL63 and SARS-CoV.
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