ArticleJournal of virology2009
Protease-mediated entry via the endosome of human coronavirus 229E.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 133 citations in OpenAlex.
- Exploring coronavirus cell entry with functional viromics.Journal of virology · 2026Review
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- The non-vesicular cholesterol transporter GRAMD1C is a pan-coronavirus antiviral target.PLoS biology · 2026Article
- Mutations to the HCoV-229E spike have counterbalancing effects on serum antibody neutralization and receptor binding.bioRxiv : the preprint server for biology · 2026Article
- Single-site mutation (M1058L) of feline infectious peritonitis virus (FIPV) spike protein in domestic cats of Northern Vietnam.Archives of virology · 2026Article
- Characterization of spike S1/S2 processing and entry pathways of lentiviral pseudoviruses bearing seasonal human coronaviruses NL63, 229E, and HKU1 spikes.Microbiology spectrum · 2025Article
- Middle East respiratory syndrome coronavirus (MERS-CoV) internalization does not rely on DPP4 cytoplasmic tail signaling.Npj viruses · 2024Article
- Human Coronavirus 229E Uses Clathrin-Mediated Endocytosis as a Route of Entry in Huh-7 Cells.Biomolecules · 2024Article
- Potential Effects of Hyperglycemia on SARS-CoV-2 Entry Mechanisms in Pancreatic Beta Cells.Viruses · 2024Review
- Jamaican fruit bat (Artibeus jamaicensis) insusceptibility to mucosal inoculation with SARS-CoV-2 Delta variant is not caused by receptor compatibility.Npj viruses · 2024Article
- Host and viral determinants of airborne transmission of SARS-CoV-2 in the Syrian hamster.eLife · 2024Article
- Structural proteins of human coronaviruses: what makes them different?Frontiers in cellular and infection microbiology · 2024Review
- Host and viral determinants of airborne transmission of SARS-CoV-2 in the Syrian hamster.bioRxiv : the preprint server for biology · 2023Article
- The Ubiquitin-Proteasome System Facilitates Membrane Fusion and Uncoating during Coronavirus Entry.Viruses · 2023Article
- Persistent immune and clotting dysfunction detected in saliva and blood plasma after COVID-19.Heliyon · 2023Article
- Convergent Evolution Dynamics of SARS-CoV-2 and HIV Surface Envelope Glycoproteins Driven by Host Cell Surface Receptors and Lipid Rafts: Lessons for the Future.International journal of molecular sciences · 2023Review
- Severe acute respiratory disease in American mink experimentally infected with SARS-CoV-2.JCI insight · 2022Article
- A Versatile Class of 1,4,4-Trisubstituted Piperidines Block Coronavirus Replication In Vitro.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Infection- or vaccine mediated immunity reduces SARS-CoV-2 transmission, but increases competitiveness of Omicron in hamsters.bioRxiv : the preprint server for biology · 2022Article
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30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human coronavirus 229E, classified as a group I coronavirus, utilizes human aminopeptidase N (APN) as a receptor; however, its entry mechanism has not yet been fully elucidated. We found that HeLa cells infected with 229E via APN formed syncytia when treated with trypsin or other proteases but not in a low-pH environment, a finding consistent with syncytium formation by severe acute respiratory syndrome coronavirus (SARS-CoV). In addition, trypsin induced cleavage of the 229E S protein. By using infectious viruses and pseudotyped viruses bearing the 229E S protein, we found that its infection was profoundly blocked by lysosomotropic agents as well as by protease inhibitors that also prevented infection with SARS-CoV but not that caused by murine coronavirus mouse hepatitis virus strain JHMV, which enters cells directly from the cell surface. We found that cathepsin L (CPL) inhibitors blocked 229E infection the most remarkably among a variety of protease inhibitors tested. Furthermore, 229E infection was inhibited in CPL knockdown cells by small interfering RNA, compared with what was seen for a normal counterpart producing CPL. However, its inhibition was not so remarkable as that found with SARS-CoV infection, which seems to indicate that while CPL is involved in the fusogenic activation of 229E S protein in endosomal infection, not-yet-identified proteases could also play a part in that activity. We also found 229E virion S protein to be cleaved by CPL. Furthermore, as with SARS-CoV, 229E entered cells directly from the cell surface when cell-attached viruses were treated with trypsin. These findings suggest that 229E takes an endosomal pathway for cell entry and that proteases like CPL are involved in this mode of entry.
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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.