Clathrin-dependent Entry of Severe Acute Respiratory Syndrome Coronavirus into Target Cells Expressing Ace2 with the Cytoplasmic Tail Deleted.
From: Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Sendai, 980-8575 Japan.
Journal of virology
- Publish Date: Aug 2007
- ISSN: 0022-538X
- Volume: 81
- Issue: 16
- Pages: 8722-9
- Medium: Print
- Language: English
- Citation (JAMA): Inoue Yuuki, Tanaka Nobuyuki, Tanaka Yoshinori, et al. Clathrin-dependent Entry of Severe Acute Respiratory Syndrome Coronavirus into Target Cells Expressing Ace2 with the Cytoplasmic Tail Deleted.. J. Virol. Aug 2007;81:8722-9
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.
Mesh Headings (Keywords): Animals, COS Cells, Cell Line, Tumor, Cercopithecus aethiops, Chlorpromazine, Clathrin, Cytoplasm, Endocytosis, Endosomes, Humans, Peptidyl-Dipeptidase A, RNA, Small Interfering, SARS Virus, Sequence Deletion, Virus Internalization
Check for Full Text / PubMed Unique Identifier (PMID): 17522231
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