作者
Nell Saunders, Ignacio Fernandez, Cyril Planchais, Vincent Michel, Maaran Michael Rajah, Eduard Baquero Salazar, Jeanne Postal, Francoise Porrot, Florence Guivel-Benhassine, Catherine Blanc, Gaëlle Chauveau-Le Friec, Augustin Martin, Ludivine Grzelak, Rischa Maya Oktavia, Annalisa Meola, Olivia Ahouzi, Hunter Hoover-Watson, Matthieu Prot, Deborah Delaune, Marion Cornelissen, Martin Deijs, Véronique Meriaux, Hugo Mouquet, Etienne Simon-Lorière, Lia van der Hoek, Pierre Lafaye, Felix Rey, Julian Buchrieser, Olivier Schwartz
发表日期
2023/12/7
期刊
Nature
卷号
624
期号
7990
页码范围
207-214
出版商
Nature Publishing Group UK
简介
Four endemic seasonal human coronaviruses causing common colds circulate worldwide: HKU1, 229E, NL63 and OC43 (ref. ). After binding to cellular receptors, coronavirus spike proteins are primed for fusion by transmembrane serine protease 2 (TMPRSS2) or endosomal cathepsins, , , , , , –. NL63 uses angiotensin-converting enzyme 2 as a receptor, whereas 229E uses human aminopeptidase-N. HKU1 and OC43 spikes bind cells through 9-O-acetylated sialic acid, but their protein receptors remain unknown. Here we show that TMPRSS2 is a functional receptor for HKU1. TMPRSS2 triggers HKU1 spike-mediated cell–cell fusion and pseudovirus infection. Catalytically inactive TMPRSS2 mutants do not cleave HKU1 spike but allow pseudovirus infection. Furthermore, TMPRSS2 binds with high affinity to the HKU1 receptor binding domain (Kd 334 and 137 nM for HKU1A and HKU1B genotypes) but not to …
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