The spike glycoprotein attached to the envelope of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to and exploits angiotensin-converting enzyme 2 (ACE2) as an entry receptor to infect pulmonary epithelial cells. A subset of integrins that recognize the arginyl–glycyl–aspartic acid (RGD) sequence in the cognate ligands has been predicted in silico to bind the spike glycoprotein and, thereby, to be exploited for viral infection. Here, we show experimental evidence that the β1 integrins predominantly expressed on human pulmonary epithelial cell lines and primary mouse alveolar epithelial cells bind to this spike protein. The cellular β1 integrins support adhesive interactions with the spike protein independently of ACE2, suggesting the possibility that the β1 integrins may function as an alternative receptor for SARS-CoV-2, which could be targeted for the prevention of viral infections.
【저자키워드】 SARS-CoV-2, angiotensin-converting enzyme 2, Cell adhesion, alveolar epithelial cells, integrin, spike 1 protein, 【초록키워드】 viral infection, ACE2, coronavirus, spike glycoprotein, in silico, viral infections, Spike protein, epithelial cells, receptor, cellular, Ligand, Interaction, pulmonary epithelial cell, Support, acute respiratory syndrome, sequence, entry receptor, experimental evidence, infect, bind, predicted, recognize, the spike protein, expressed, subset, alveolar epithelial cell, 【제목키워드】 spike, surface, bind,