COVID project

In our original research article entitled "Less severe endothelial injury and vascular pathway activation in SARS-CoV-2 omicron variant compared to alpha" we aimed at assessing the impact of viral infections with different disease severity on the endothelium, especially in a changing affected population (mostly vaccinated, infected with new viral variants). We included COVID-19 hospitalized patients, mostly vaccinated and infected with SARS-CoV-2 omicron variant, to characterize their endothelial involvement and compare it with SARS-CoV-2 alpha infection.
We quantified circulating endothelial cells and assessed their ACE2 surface expression in patients and controls. In vitro, we evaluated the endothelial toxicity of SARS-CoV-2 omicron serum, NF-κB activation, and performed plasma proteomic profiling, comparing findings with alpha variant-infected subjects. Our results indicate that omicron infection is associated with ongoing endothelial injury, but without significant in vitro endothelial toxicity or NF-κB activation. Both variants alter key vascular homeostasis proteins (IL-6, TRAIL-R2); however, alpha strain induces greater cytokine release and activates distinct pathways (PARP1, Renin-Angiotensin System), sustaining a “vasculoinflammatory” loop.
Patients infected with SARS-CoV-2 during 2022—predominantly with the omicron variant and vaccinated—exhibit evidence of acute endothelial injury, without inducing significant endothelial toxicity in vitro. Comparative analysis of omicron and alpha variant infections highlights key mediators of cardiovascular homeostasis, suggesting potential therapeutic targets for improving cardiovascular prevention during viral infections.