~~~~~~~~~~~~~~~
"created by Virginia Tech's University Distinguished Professor X.J. Meng "
Meng Laboratory: Dr. Meng's CV (vt.edu)
Firing Squad or Electric Chair? /ba-dum t’sssh>
SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: Implications for microclot formation in COVID-19 Questions: can clots resultant from spike protein, be differentiated chemically from pre-COVID thromoboses (e.g. a-fib, genetic, idiopathic?)
If the clotting mechanism is subtly different, or the chemical substrate of the clot is different, does this suggest that certain classes of blood thinners are to be preferred over others? Is it possible to artificially stimulate the body's slow natural breakdown of clots?
Is there more than one process the body uses for breaking down clots?
If so, are any of these processes more efficacious for COVID-clots than others (assuming for the nonce, that COVID clots are chemically distinguishable from non-COVID...)?
Are there any drugs or OTC supplements which would tend to interfere with the pathway by which the spike protein induces clotting?
Any hematologists on board, who will do more than parrot the party line ("Blame Trump and white people and take your mRNA jab! Because SCIENCE!"™) ?