Scientists identify abnormal blood-clotting mechanism in long COVID patients, study reports

ISTANBUL

New research has uncovered unusual blood changes in long COVID patients, revealing interactions between tiny clots and altered immune cells that scientists say could help explain the condition’s persistent symptoms.

The study, published in the Journal of Medical Virology, found that long COVID patients show significantly higher levels of “microclots," abnormal clumps of blood-clotting proteins, as well as increased formation of structures called neutrophil extracellular traps (NETs), which are released by white blood cells to trap pathogens.

Researchers say the interaction between these microclots and NETs may be driving widespread inflammation and prolonged COVID-like symptoms such as fatigue, brain fog, pain, and breathlessness.

“These findings suggest underlying physiological interactions between microclots and NETs that, when dysregulated, may become pathogenic,” said Alain Thierry of the Montpellier Cancer Research Institute, a co-author of the study.

Neutrophils in long COVID patients were found to undergo changes that cause them to expel DNA and enzymes, forming NETs that scientists believe may stabilize and enlarge microclots, preventing the body from breaking them down.

“We suggest that higher NETs formation might promote the stabilisation of microclots in circulation, potentially leading to deleterious effects which contribute causally to the long Covid syndrome,” researchers wrote.

The study compared blood plasma from long COVID patients with that of healthy volunteers, noting that microclots in patients were not only more abundant but also larger.

Scientists say the findings provide new insight into the biological mechanisms behind long COVID and could pave the way for targeted treatment approaches focused on reducing microclot formation or limiting NET activity.