Figure 2.

The potential role of NETs in long COVID may involves multiple pathways. NETs have been shown to drive pro-fibrotic responses in the alveolar epithelium and lung fibroblasts, leading to lung fibrosis. An array of autoantibodies detected in long COVID, including anti-NET IgM and IgG, which have been shown to protect NETs against degradation, contributing to downstream inflammation, vascular damage, and thrombosis. NETs are known to contribute to atherosclerosis and myocardial inflammation, perhaps explaining the cardiovascular sequelae in long COVID patients. Neuropsychiatric abnormalities in long COVID are associated with neuroinflammation and blood-brain barrier disruption, which can be induced by neutrophil-endothelial cell interactions and NET production. This Figure was created using BioRender.com.