Microclots in Fluorescence Microscopy, thromboelastography® (TEG®)
- SARS-CoV-2 spike protein induces abnormal inflammatory blood clots neutralized by fibrin immunotherapy
- Clogged Pipes and Microclots
- Long COVID and the role of fibrin amyloid (fibrinaloid) microclots: http://dbkgroup.org/longcovid/ –
- hard-to-remove fibrin amyloid microclots (also containing other proteins), that can inhibit blood flow to capillaries and hence O2 transfer to tissues, are involved in, and can account for, most (if not all) of the symptoms of Long COVID
- Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin –
- Plasma samples from Long COVID/PASC still contain large anomalous (amyloid) deposits (microclots). – These microclots in both acute COVID-19 and Long COVID/PASC plasma samples are resistant to fibrinolysis (compared to plasma from controls and T2DM), even after trypsinisation.
- After a second trypsinization, the persistent pellet deposits (microclots) were solubilized – Various inflammatory molecules are substantially increased in both the supernatant and trapped in the solubilized pellet deposits of acute COVID-19 and Long COVID/PASC – Substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits