Breaking: New PolyBio-supported Study Identifies Microclots, Endothelial Injury Markers and Neutrophil Activation in Children and Young Adults with Long COVID
A new study supported by PolyBio Research Foundation studied children and young adults with Long COVID, providing evidence linking endovascular inflammation, increased quantity and size of fibrin-amyloid “microclots,” and neutrophil activation, and finding detectable Spike protein in a subset.
polybio.org/new-study-poly…
2/ Published in Pediatric Research, the study helps clarify the biological basis of cardiovascular symptoms in an important but understudied Long COVID population, and advances scientific insights that will support future diagnostic development.
nature.com/articles/s4139…
3/ “Given that children and adults can have significantly different responses to acute COVID-19 illness, it’s important to study, understand, and document Long COVID-related biological changes in children and young adults,” said Michael VanElzakker PhD, PolyBio co-founder, neuroscientist at Massachusetts General Hospital/Harvard Medical School, and an author on the study.
4/ The study investigators enrolled 84 children and young adults from the United States and Canada, including 61 participants with Long COVID and 23 healthy pediatric controls, and analyzed symptom burden alongside blood-based markers of vascular dysfunction.
5/ From the paper: Children and young adults with long COVID have altered levels and strong associations between circulating endovascular-associated cytokines. a Correlation matrix between 32 endothelial cytokines in Long COVID patients.
6/ The team found that participants with Long COVID had a significantly increased burden of fibrin amyloid microclots in the blood. They also observed abnormal endothelial signaling, including increased markers of angiogenesis and vascular remodeling such as FGF-2, which correlated with microclot burden.
7/ At the same time, cell-free DNA – a marker consistent with intravascular neutrophil extracellular trap formation, or NETosis – was elevated and positively correlated with serum amyloid A, a component of microclots. FGF-2, a cytokine involved in angiogenesis and wound healing, was significantly increased in Spike-positive versus Spike-negative patients.
8/ Importantly, the study went beyond correlation. In vitro co-culture assays showed that SARS-CoV-2 Spike protein immune complexes can trigger NETosis, which in turn contributes to endothelial injury. Taken together, the findings suggest that intravascular neutrophil activation may be a key driver of endovascular pathology in Long COVID.
9/ The pediatric and young adult focus of the study is especially important. Because younger individuals are less likely to have the cardiometabolic and inflammatory comorbidities that often complicate interpretation in older adult cohorts, these findings strengthen the case that microclots and endothelial abnormalities are directly related to Long COVID biology rather than background age-related disease.
10/ The team proposes that a combination of microclots, neutrophil markers, endothelial cytokines, and potentially circulating Spike protein could serve as biomarkers for Long COVID – an advance that could help support more rigorous diagnosis, patient stratification, and assessment of therapeutic response in future studies.
11/ For PolyBio, the study underscores a central principle: Long COVID is not a vague syndrome but a condition with measurable biological drivers. By supporting work that identifies objective markers of disease, PolyBio is helping build the scientific foundation for the next generation of Long COVID diagnostics and targeted clinical trials.
polybio.org/new-study-poly…
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