ArticleJournal of virology2007
Clathrin-dependent entry of severe acute respiratory syndrome coronavirus into target cells expressing ACE2 with the cytoplasmic tail deleted.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 256 papers, 1 of them a synthesis that pooled it.
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Who cites it
256 citing papers in PubMed, 1 synthesis or guideline pooled it, 391 citations in OpenAlex.
- The Role of Host Genetic Factors in Coronavirus Susceptibility: Review of Animal and Systematic Review of Human Literature.American journal of human genetics · 2020Pooled it
- Article
- Coronavirus Nsp3 Hijacks CLTC to Modulate Autophagosome Nucleation for Promoting DMV Formation and Viral Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Combined ACEI and ARB therapy and ICU mortality in critically ill COVID-19 patients: a retrospective cohort study.Frontiers in pharmacology · 2026Article
- Placental infection by SARS-CoV-2: exploring alternative entry pathways.Tissue barriers · 2026Article
- Bovine coronavirus enters HRT-18 cells via membrane fusion and clathrin-mediated endocytosis in a low pH-, dynamin-, cholesterol-, microtubule-, Rab7-, and Rab11-dependent manner.Journal of virology · 2025Article
- Automated Label-Free Assay for Viral Detection and Inhibitor Screening via Biomembrane-Functionalized Microelectrode Arrays.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Evolution of the SARS-CoV-2 spike protein in utilizing host transmembrane serine proteases.iScience · 2025Article
- Fluidic shear stress alters clathrin dynamics and vesicle formation in endothelial cells.Biophysical journal · 2025Article
- RNASEK interacting with PEDV structural proteins facilitates virus entry via clathrin-mediated endocytosis.Journal of virology · 2025Article
- Dual role of ACE2 in regulating inflammation triggered by Omicron S1 and other SARS-CoV-2 Spike variants.Frontiers in immunology · 2025Article
- Article
- Article
- 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
- A dual inhibitor of PIP5K1C and PIKfyve prevents SARS-CoV-2 entry into cells.Experimental & molecular medicine · 2024Article
- Reduction in ACE2 expression in peripheral blood mononuclear cells during COVID-19 - implications for post COVID-19 conditions.BMC infectious diseases · 2024Article
- Recreating the biological steps of viral infection on a cell-free bioelectronic platform to profile viral variants of concern.Nature communications · 2024Article
- Inhibition of endocytic uptake of severe acute respiratory syndrome coronavirus 2 and endo-lysosomal acidification by diphenoxylate.Antimicrobial agents and chemotherapy · 2024Article
196 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
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The penetration of various viruses into host cells is accomplished by hijacking the host endocytosis machinery. In the case of severe acute respiratory syndrome coronavirus (SARS-CoV) infection, viral entry is reported to require a low pH in intracytoplasmic vesicles; however, little is known about how SARS-CoV invades such compartments. Here we demonstrate that SARS-CoV mainly utilizes the clathrin-mediated endocytosis pathway for its entry to target cells by using infectious SARS-CoV, as well as a SARS-CoV pseudovirus packaged in the SARS-CoV envelope. The SARS-CoV entered caveolin-1-negative HepG2 cells, and the entry was significantly inhibited by treatment with chlorpromazine, an inhibitor for clathrin-dependent endocytosis, and by small interfering RNA-mediated gene silencing for the clathrin heavy chain. Furthermore, the SARS-CoV entered COS7 cells transfected with the mutant of ACE2 with the cytoplasmic tail deleted, SARS-CoV receptor, as well as the wild-type ACE2, and their entries were significantly inhibited by treatment with chlorpromazine. In addition, ACE2 translocated into EEA1-positive early endosomes immediately after the virus attachment to ACE2. These results suggest that when SARS-CoV binds ACE2 it is internalized and penetrates early endosomes in a clathrin-dependent manner and that the cytoplasmic tail of ACE2 is not required for the penetration of SARS-CoV.
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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.