Fig. 6.

Vimentin concentration in detrimental saliva is associated with enhanced in vitro SARS-CoV-2 infectivity. (A) The effect of increasing concentrations of recombinant proteins on relative SARS-CoV-2 infection of VeroE6 cells (n = 3; ** = p < 0.005, analysis of variance). (B) Predicted effect of target proteins on relative infection of VeroE6 cells for vimentin abundances in Group C (detrimental) saliva samples as calculated from mass spectrometry (n = 10). (C) Immunofluorescence staining of infected air-liquid interface airway epithelial cells, with cell nuclei (red), spike antigen (blue) and vimentin (white), and a plot of signal co-localization between SARS-CoV-2 spike and cellular vimentin. (D) Graphical representation of proposed mechanisms for enhanced viral entry caused by vimentin. Left panel shows that surface-expressed vimentin may act as a co-receptor for SARS-CoV-2 and ACE2 binding to promote viral entry. Right panel shows extracellular vimentin in mucosal secretions such as saliva may bind to SARS-CoV-2 via the spike protein, stabilizing binding interactions with ACE2 during cell infection. Created with Biorender.com. ACE2 = angiotensin-converting enzyme 2.