生物
病毒
严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)
免疫学
2019年冠状病毒病(COVID-19)
欧米林
2019-20冠状病毒爆发
作者
James L. Daly,Boris Simonetti,Katja Klein,Kai-En Chen,Maia Kavanagh Williamson,Carlos Antón-Plágaro,Deborah K. Shoemark,Lorena Simón-Gracia,Michael Bauer,Reka Hollandi,Urs F. Greber,Peter Horvath,Richard B. Sessions,Ari Helenius,Julian A. Hiscox,Tambet Teesalu,David A. Matthews,Andrew D. Davidson,Brett M. Collins,Peter J. Cullen,Yohei Yamauchi
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2020-11-13
卷期号:370 (6518): 861-865
被引量:515
标识
DOI:10.1126/science.abd3072
摘要
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), uses the viral spike (S) protein for host cell attachment and entry. The host protease furin cleaves the full-length precursor S glycoprotein into two associated polypeptides: S1 and S2. Cleavage of S generates a polybasic Arg-Arg-Ala-Arg carboxyl-terminal sequence on S1, which conforms to a C-end rule (CendR) motif that binds to cell surface neuropilin-1 (NRP1) and NRP2 receptors. We used x-ray crystallography and biochemical approaches to show that the S1 CendR motif directly bound NRP1. Blocking this interaction by RNA interference or selective inhibitors reduced SARS-CoV-2 entry and infectivity in cell culture. NRP1 thus serves as a host factor for SARS-CoV-2 infection and may potentially provide a therapeutic target for COVID-19.
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