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!"™) ?
Holy crap.
A singular spike protein is between 180–200 kDa in size and contains an extracellular N-terminal, a transmembrane domain fixed in the membrane of the virus, and a short intracellular C-terminal segment (Kawase et al., 2019, Zhang et al., 2020). Spike proteins are coated with polysaccharide molecules that serve as camouflage. This helps evade surveillance by the host immune system during entry (Zhang et al., 2020).
So their cure for the c00f is to inject mRNA for a protein which
a) attaches to the ACE2 receptor which causes all kinds of pro-inflammatory chemical signals to be sent (from other links I've sent recently, not in this paper)
b) from THIS paper, promotes clots which are resistant to fibrolysis
c) from THIS paper, is resistant to recognition by the immune system.
F. this S.
Fauci funded the gain of function research.
Fauci is pushing the mRNA jabs.
You fill in the rest.