期刊
VIROLOGICA SINICA
卷 37, 期 3, 页码 380-389出版社
KEAI PUBLISHING LTD
DOI: 10.1016/j.virs.2022.03.003
关键词
SARS-CoV-2; Endocytosis; Phosphoinositides; Angiotensin converting enzyme 2 (ACE2); Syncytium
类别
This study demonstrates that the entry of SARS-CoV-2 into host cells depends on clathrin-mediated endocytosis, with phosphoinositides playing essential roles in this process. The intracellular domain and catalytic activity of ACE2 are not required for efficient virus entry, and the Delta variant also enters cells through clathrin-mediated endocytosis.
The recent COVID-19 pandemic poses a global health emergency. Cellular entry of the causative agent SARS-CoV-2 is mediated by its spike protein interacting with cellular receptor-human angiotensin converting enzyme 2 (ACE2). Here, by using lentivirus based pseudotypes bearing spike protein, we demonstrated that entry of SARS-CoV-2 into host cells was dependent on clathrin-mediated endocytosis, and phosphoinositides played essential roles during this process. In addition, we showed that the intracellular domain and the catalytic activity of ACE2 were not required for efficient virus entry. Finally, we showed that the current predominant Delta variant, although with high infectivity and high syncytium formation, also entered cells through clathrin-mediated endocytosis. These results provide new insights into SARS-CoV-2 cellular entry and present proof of principle that targeting viral entry could be an effective way to treat different variant infections.
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