Westman et al. (2025)
- Authors: Henrik Westman, Per Hammarström, Sofie Nyström
- Institutes: Department of Physics, Chemistry, and Biology (IFM), Linköping University, Linköping, Sweden, SciLifeLab, Linköping University, Linköping, Sweden
- Publisher: Biochemistry
- Link: DOI
Summary
This research provides a direct molecular explanation for the ‘fibrinaloids’ or microclots found in Long COVID and ME/CFS patients. By demonstrating that specific fragments of the SARS-CoV-2 Spike protein create clots that are physically resistant to the body’s natural breakdown mechanisms, the study validates a major theory of the disease’s vascular pathology. These findings offer a potential diagnostic marker and suggest that treatments targeting these specific amyloid-protein interactions could help restore normal blood flow and reduce systemic symptoms. Overall, it identifies a clear mechanism for why viral remnants can cause long-term health issues long after the initial infection.
What was researched?
This study investigated how specific amyloid-forming peptides from the SARS-CoV-2 Spike protein interact with and disrupt the human blood coagulation system.
Why was it researched?
The researchers aimed to understand the molecular cause of ‘fibrinaloids,’ or amyloid microclots, which are thought to contribute to persistent inflammation and circulatory issues in patients suffering from post-viral conditions.
How was it researched?
The team tested seven amyloidogenic Spike protein fragments in a controlled laboratory environment using purified clotting proteins. They monitored how these fragments affected the formation of fibrin clots and their subsequent breakdown after adding the enzyme activator tPA 💊.
What has been found?
Two specific fragments, Spike601 and Spike685, were found to be highly active in disrupting the clotting process. Spike601 interfered with initial clot formation, while Spike685 caused the creation of dense, abnormal clot networks that were essentially immune to being dissolved by natural enzymatic processes.
Discussion
While the study was limited to laboratory conditions using isolated components, it provides strong evidence for the amyloid-microclot hypothesis. The identification of specific ‘active’ peptides offers a focused pathway for future clinical research into treating the vascular symptoms of Long COVID and ME/CFS.
Conclusion & Future Work
The study concludes that specific Spike protein amyloid fibrils can directly cause the formation of lysis-resistant microclots. These results explain how viral proteins could contribute to the systemic vascular pathology observed in persistent post-viral diseases.