Table 1 Integrins expression involved with SARS‐CoV‐2 infection

αvβ3

Expressed throughout the host, particularly in the endothelium.

SARS-CoV-2 caused vascular dysregulation in vitro during COVID-19 via major endothelial integrin αvβ3 to.⁴¹³

αvβ6

A molecular target and an epithelium-specific cell-surface receptor, that is upregulated in injured tissues, including fibrotic lung.

αvβ6 Integrin, an intriguing target for both the inhibition of SARS-CoV-2 entry and the diagnosis/treatment of COVID-19-related fibrosis.⁴⁰⁶ PET/CT images using the integrin αvβ6-binding peptide (18F-αvβ6-BP), as an approach to identify the presence, persistence, and progression of lung damage.⁴¹⁶

αvβ8

Expressed via epithelial cells and fibroblasts in the lung.

The high expression of integrin in the lung and its high binding affinity to viral RGD motif (~KD = 4.0 nM) may be the possible reasons for the high infectivity of SARS-CoV-2.⁴¹⁷

αIIbβ3

Expressed on the surface of platelets, and it plays an important role in platelet aggregation and blood clotting.

The integrin αIIbβ3-based platelet activation status declined in nonsurvivors compared to survivors in COVID-19 patients.⁴¹⁸

α5β1

Expressed in the fetal lung mesenchyme.

Blockade of SARS-CoV-2 binding to integrins α5β1 and αvβ3 by the small peptides ATN-161 and Cilengitide reduced viral infectivity and attenuate vascular inflammation.⁴¹⁹ The S protein of SARS-CoV-2 induces endothelial inflammation by signaling of integrin α5β1 and NF-κB.⁴²⁰

α4β7

Expressed on memory CD4⁺ T cells.

COVID-19 is associated with a decrease of the key gut-homing marker α4β7 in circulating adaptive immune cells.⁴²¹