Evaluation of a point of care lateral flow assay for antibody detection following SARS CoV-2 mRNA vaccine series.

BACKGROUND: Breakthrough cases of SARS-CoV-2 infection correlate with decreased antibody immunity following mRNA vaccination. Measuring kinetics of vaccine efficacy using traditional laboratory approaches is more expensive and can be impractical. In this study, we evaluated the diagnostic performance of a validated COVID-19 point-of-care lateral flow assay (LFA) kit in detecting post-vaccination antibody response. METHODS: We conducted a prospective cohort study of whole blood and plasma samples to evaluate the performance of a LFA in detecting SARS-CoV-2-specific antibodies following mRNA vaccination compared to enzyme-linked immunosorbent assays (ELISAs). Health care workers at 2 tertiary centers who completed an initial BNT162b2 (n = 103) or mRNA-1273 (n = 35) vaccine series were enrolled between June and August of 2021. We performed an exploratory analysis to correlate band strength and antibody concentration of LFAs and ELISAs respectively. RESULTS: When compared to the ELISA, LFA results showed similar test positivity for plasma samples (P = 0.55), but not for whole blood samples (P < 0.001). For whole blood samples on the LFA, antibody detection differed between BNT162b2 (68.9%, 95% CI: 59.1%-77.7%) and mRNA-1273 (100%, 95% CI: 90.0%-100%, P < 0.001) vaccines. Higher plasma antibody concentrations correlated with greater LFA sensitivity. Samples with thick LFA bands had higher antibody concentrations compared to samples having faint LFA bands (81.8 arbitrary unit [AU]/mL vs. 57.1 AU/mL, P < 0.01). CONCLUSIONS: The performance of a LFA in detecting SARS-CoV-2 antibodies was significantly better when plasma samples were used. The strength of label bands on the LFA may correlate with antibody concentration and could be a useful point-of-care monitoring tool for post-vaccine antibody status.

COVID-19-associated Lung Microvascular Endotheliopathy: A "From the Bench" Perspective.

Rationale: Autopsy and biomarker studies suggest that endotheliopathy contributes to coronavirus disease (COVID-19)-associated acute respiratory distress syndrome. However, the effects of COVID-19 on the lung endothelium are not well defined. We hypothesized that the lung endotheliopathy of COVID-19 is caused by circulating host factors and direct endothelial infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Objectives: We aimed to determine the effects of SARS-CoV-2 or sera from patients with COVID-19 on the permeability and inflammatory activation of lung microvascular endothelial cells. Methods: Human lung microvascular endothelial cells were treated with live SARS-CoV-2; inactivated viral particles; or sera from patients with COVID-19, patients without COVID-19, and healthy volunteers. Permeability was determined by measuring transendothelial resistance to electrical current flow, where decreased resistance signifies increased permeability. Inflammatory mediators were quantified in culture supernatants. Endothelial biomarkers were quantified in patient sera. Measurements and Main Results: Viral PCR confirmed that SARS-CoV-2 enters and replicates in endothelial cells. Live SARS-CoV-2, but not dead virus or spike protein, induces endothelial permeability and secretion of plasminogen activator inhibitor 1 and vascular endothelial growth factor. There was substantial variability in the effects of SARS-CoV-2 on endothelial cells from different donors. Sera from patients with COVID-19 induced endothelial permeability, which correlated with disease severity. Serum levels of endothelial activation and injury biomarkers were increased in patients with COVID-19 and correlated with severity of illness. Conclusions: SARS-CoV-2 infects and dysregulates endothelial cell functions. Circulating factors in patients with COVID-19 also induce endothelial cell dysfunction. Our data point to roles for both systemic factors acting on lung endothelial cells and viral infection of endothelial cells in COVID-19-associated endotheliopathy.