by Daniel Brouse
Originally, COVID-19 was thought to be a respiratory infection. It didn’t take long to discover that SARS-CoV-2 quickly enters the heart, blood stream, and can infect every organ.
Now we know that SARS-CoV-2 causes micro bloodclots that do not necessarily clear the system.
Resta Pretorius, a South African scientist, says, “When we speak about long COVID and microclots, I think we should just step back a second and speak about acute COVID. We have noted – we and others have noted that the vascular system and clotting is not working properly during acute COVID. So the dilemma with long COVID is that the percentage of individuals, up to 30%, never really get over the presence of these clotting abnormalities or physiological abnormalities when they are not infective anymore – so when they get over the normal five to 10 days of acute COVID. So during long COVID, these clots then just continue to be present.”
“Inside the microclots that are present in these individuals’ blood in circulation, there are various entrapped molecules, inflammatory molecules, that actually prevent the breakdown of the microclots. So although the body’s trying very hard to break down these clots with the normal physiological processes, molecules entrapped in the microclots actually prevent it from breaking down.”
“Now, that is a massive issue because if these microclots are in circulation, it damages the vasculature, or your blood vessels, and in that process, prevents the cells to receive enough oxygen, causing then a failure of the coagulation system of oxygen to your cells. And that can be linked to all of the lingering symptoms that have been noted in long COVID.”
The Results of Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin: We show that plasma samples from Long COVID/PASC still contain large anomalous (amyloid) deposits (microclots). We also show that 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. We detected various inflammatory molecules that are substantially increased in both the supernatant and trapped in the solubilized pellet deposits of acute COVID-19 and Long COVID/PASC, versus the equivalent volume of fully digested fluid of the control samples and T2DM. Of particular interest was a 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.
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