Cross-sectional study comparing immune and endothelial cell dysfunction in adults with Long COVID (n=73) vs. age- and sex-matched infection-recovered controls (n=41), using spectral flow cytometry to assess necroptosis (pMLKL), autophagy (LC3), hypoxia (HIF1-α), and NET markers, alongside clinical autonomic and vascular measures.
Long COVID patients had significantly higher symptom scores, impaired heart rate variability, and reduced endothelial reactivity. Circulating endothelial cells (CECs) were markedly elevated and showed increased necroptosis and autophagy activation; elevated pMLKL in CECs strongly correlated with symptom severity and autonomic dysfunction. Monocyte-platelet and CEC-platelet aggregates were increased, indicating a prothrombotic state.
Cross-sectional design limits causal inference. No data on prior vaccination status, COVID variant, or time since acute infection. Mechanistic findings are associative; no therapeutic intervention was tested.
Long COVID patients show measurable endothelial and immune cell stress via necroptosis and autophagy pathways that track with symptom burden and dysautonomia. Clinicians should be aware that vascular and autonomic dysfunction in Long COVID may have identifiable cellular correlates, and necroptosis-targeting therapies warrant future investigation.
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