Long COVID as Vascular Homeostatic Failure A Falsifiable Systems Hypothesis Using Human–AI Teaming Intelligence (HATI)

Long COVID presents as a heterogeneous, multisystem condition for which no single unifying mechanism has been established. This paper proposes and evaluates a falsifiable systems hypothesis in which a subset of Long COVID cases may involve persistent vascular homeostatic dysfunction associated with neutrophil extracellular traps (NETs) and fibrinolysis-resistant microclots. Drawing on recent peer-reviewed findings, the paper reframes these observations not as proof of causation, but as evidence of regulatory failure following acute infection. The work explicitly addresses heterogeneity, uncertainty, and competing mechanisms including viral persistence and autoimmunity, and defines clear criteria by which the hypothesis could be falsified. Human–AI Teaming Intelligence (HATI) is used as a collaborative synthesis framework rather than a diagnostic or clinical system. This paper does not propose treatments, clinical protocols, or medical advice, and is intended solely as a research-stage conceptual contribution.