A Sci Nature News post revived a dramatic claim: “People with COVID now have sticky micro-clots in their blood.” The claim echoes a paper published on Oct. 2, 2025, so the research is not a new discovery in October 2026. More importantly, the study examined people with long COVID, not everyone with an active or past coronavirus infection.
What the researchers found
The Journal of Medical Virology study compared plasma from 50 people with long COVID and 38 healthy controls. Researchers used imaging flow cytometry and fluorescence microscopy to count fibrin(ogen) amyloid particles, which the paper calls microclots, and measure markers linked to neutrophil extracellular traps, or NETs.
Long-COVID samples contained more of the particles, and their number and size were associated with levels of myeloperoxidase, neutrophil elastase and circulating nuclear DNA. Microscopy also showed NET-related material in or around some particles. The authors proposed that excess NET formation might help stabilize the particles and contribute to long COVID.
That last step is a hypothesis. The study found an association in blood samples; it did not demonstrate that the particles caused participants’ symptoms, blocked their capillaries, deprived their tissues of oxygen or produced brain damage. It also did not test a treatment. Several authors disclosed patents related to inflammatory-disease or long-COVID diagnostics, and some were affiliated with Biocode Technologies.
Why the evidence remains unsettled
A 2023 Cochrane review reached a cautious conclusion about earlier research. It found that similar amyloid fibrin(ogen) particles appeared in healthy people and in people with other diseases, and that the available laboratory evidence could not show that the particles contribute to post-COVID condition.
That review searched studies only through October 2022, so it does not evaluate the 2025 paper. The newer work adds quantitative and structural evidence linking the particles with NET markers in long COVID, but a small observational comparison still cannot confirm a causal mechanism.
The post reduces that nuance to a universal claim about “people with COVID.” The paper supports a narrower conclusion: one long-COVID cohort had more fibrin(ogen) amyloid particles and related inflammatory markers than healthy controls. Whether those findings explain symptoms, apply broadly or point to an effective treatment still requires independent research.
