10/16/2026
Long COVID is characterized by persistent symptoms following SARS-CoV-2 infection and has been linked to abnormal thromboinflammatory processes in the blood.
Individuals with the condition show substantially higher numbers and larger sizes of circulating microclots, which are amyloid-like fibrin aggregates small enough to obstruct capillary flow yet resistant to normal breakdown.
These microclots coexist with elevated neutrophil extracellular traps, or NETs, which are web-like DNA and protein structures extruded by neutrophils to capture pathogens.
Recent investigations demonstrate a previously unreported structural association in which NETs become physically embedded within the microclots.
This embedding is present in healthy blood as well but is markedly more pronounced among Long COVID patients.
The sticky NET mesh appears to stabilize the fibrin structures, shielding them from fibrinolysis, the enzymatic process that normally dissolves clots.
As a result, microclots persist longer in the circulation, potentially impairing microvascular perfusion, reducing oxygen delivery to tissues, and contributing to chronic endothelial injury.
Markers of both microclots and NETs correlate strongly with each other and exhibit high diagnostic accuracy in distinguishing patients from controls.
These observations point to a dysregulated interaction between immune-derived NETs and fibrin amyloid particles that may help drive the microvascular complications and lingering symptoms of Long COVID.
Source: Thierry AR, et al. Circulating Microclots Are Structurally Associated With Neutrophil Extracellular Traps and Their Amounts Are Elevated in Long COVID Patients. Journal of Medical Virology. 2025;97(10):e70613. DOI: 10.1002/jmv.70613.