Scientists have identified a persistent change in a handful of blood proteins in people with long Covid that indicates that an important part of their immune system remains on high alert for months after an acute infection.
The study followed 113 Covid patients for up to one year after they were first infected, along with 39 healthy controls. At the six-month mark, 40 patients had developed long Covid symptoms.
Repeated blood samples turned up important differences in their blood: A group of proteins indicated that a part of the body’s immune system called the complement system remained activated long after it should have returned to normal.
Or shouldn’t it? Maybe the immune system keeps seeing something not to be named?
“When you have a viral or bacterial infection, the complement system becomes activated and binds to these viruses and bacteria and then eliminates them,” said Dr. Onur Boyman, a professor of immunology at the University of Zurich in Switzerland and one of the study’s investigators. The system then returns to its resting state, where its regular job is to clear the body of dead cells, he said. But if the complement system remains in its microbe-fighting state after the viruses and bacteria are eliminated, “it starts damaging healthy cells,” he said.
And wasn’t it what they were told all the way before the mRNA jabs were even deployed to transfect billions upon billions of jabbenee’s cells with the mRNA code that would produce the modified S spike protein to be displayed on the surface of these cells and also spread around the body via exosome shedding by the transfected cells? Why act surprised after the fact?
Lingering symptoms persist for as much as 6 months (or longer) after acute infection, where COVID-19 survivors complain of recurring fatigue or muscle weakness, being out of breath, sleep difficulties, and anxiety or depression. Given that blood clots can block microcapillaries and thereby inhibit oxygen exchange, we here investigate if the lingering symptoms that individuals with Long COVID/PASC manifest might be due to the presence of persistent circulating plasma microclots that are resistant to fibrinolysis.
Mass spectrometry was performed using a Thermo Scientific Fusion mass spectrometer equipped with a Nanospray Flex ionization source. Plasma samples, before and after addition of spike protein addition (1 ng mL−1 final exposure concentration), from4 of our control samples were analysed with this method.
Results: 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.
And that was the only time the cited study contains the word “spike” (probably demanded by the editors of Cardiovasc Diabetol.), although all of the study then goes on to demonstrate that the spike is the reason for the micro-clotting and amyloid fibrin formation.
Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection, the cause of coronavirus disease 2019 (COVID-19), is characterized by unprecedented clinical pathologies. One of the most important pathologies, is hypercoagulation and microclots in the lungs of patients. Here we study the effect of isolated SARS-CoV-2 spike protein S1 subunit as potential inflammagen sui generis. Using scanning electron and fluorescence microscopy as well as mass spectrometry, we investigate the potential of this inflammagen to interact with platelets and fibrin(ogen) directly to cause blood hypercoagulation.
Using platelet-poor plasma (PPP), we show that spike protein may interfere with blood flow. Mass spectrometry also showed that when spike protein S1 is added to healthy PPP, it results in structural changes to β and γ fibrin(ogen), complement 3, and prothrombin. These proteins were substantially resistant to trypsinization, in the presence of spike protein S1. Here we suggest that, in part, the presence of spike protein in circulation may contribute to the hypercoagulation in COVID-19 positive patients and may cause substantial impairment of fibrinolysis. Such lytic impairment may result in the persistent large microclots we have noted here and previously in plasma samples of COVID-19 patients.
Persistent large microclots, eh?
Back to the newest discovery - instead of testing for S spike in circulation, persistent microclots and red blood cell levels (deficiency), the study proposes a new biomarker in a form of a C5bC6/C7 complex ratio of the complement activation system (“our observation of increased complement activity in the presence of elevated C5bC6 levels and decreased soluble C7 complexes suggested increased membrane insertion of TCCs in active Long Covid”), as the immune system went off rails in Long Covid subjects, trying to mop up the damage being continuously caused by the produced and circulating S spike? What a perversion! On the other hand, the slides in this study are most artful and beautiful, if you read studies for aesthetic reasons:
At this rate the $cience will stay baffled for decades. Just as the doctor ordered.
I didn't see a mention of how many covid shots the "long covid" study participants had received.
Long cv, a method to publish without mentioning the vx produced spikeprotein. Regardless publications should be read with skepticism.