“A possible new diagnostic approach to Long COVID. Long COVID may involve microcirculatory blockages - tiny, persistent clots known as fibrinaloid microclots. These abnormal fibrin structures resist breakdown and can obstruct blood flow in the smallest vessels.🧵”
Stellenbosch University and Montpellier researchers studied 50 Long COVID patients and found their blood carried far more microclots tied to neutrophil immune traps.
These sticky structures may stabilize clots and help explain persistent symptoms.
A new study shows that adding SARS-CoV-2’s main protease (Mpro) enzyme to plasma from healthy donors can trigger blood clots by activating coagulation factors VII and XII.
This may explain Covid’s common blood clot risk.
“SARS-CoV-2 hijacks the clotting system of your body for its own purposes.
The spike protein binds to fibrin, rendering it toxic. Those toxic fibrin proteins damage blood vessel walls and drive an inflammatory response.
Other viruses don't do this.”
“I’ve never seen patients in their 20’s and 30’s with DVT’s until the past few years. It’s unspeakably messed up.
Not too long ago, saw yet another, this time un-vax’d.
@RandPaul End gain of function and have Nuremberg trials for the sociopaths who did this.”
“Findings emphasize that Covid-19’s myocardial pathology predominantly arises from fibrin thrombi within the coronary MICROVASCULAR network, especially in the abluminal spaces.
➡️This pathological process leads to myocardial fibre injury, necrosis, and ischemic changes( = fibrosis), contributing to both the acute symptoms and long-term sequelae (Long Covid).”
Using stem-cell-derived vascular cells, researchers found SARS-CoV-2 infects smooth muscle cells (SMCs), not endothelial cells.
Infected SMCs cause inflammation and clotting factors, explaining vascular issues seen in severe COVID-19 cases.
“About 20% of my young patients are showing evidence of increased clotting as part of the baseline lab panels.
Never used to see this.”
“Medical images show us that the severe lung disease of #COVID-19 is the opposite of influenza - it occupies a different anatomical compartment in the lungs. All of this means there is no reason to expect that the later phases of COVID-19 should be anything like influenza.”
“Navigating social distancing requirements that complicated lab work, Akassoglou and her collaborators conducted a series of experiments in mice to explore the pernicious role of the coronavirus’s spike protein.
They discovered that beyond serving as the virus’s “key” to enter cells, spike binds with a blood clotting factor called fibrinogen, creating structurally abnormal, inflammation-promoting clumps of fibrin — the insoluble material that forms the mesh-like structures essential for wound healing.
High levels of these abnormal clots not only push the body’s clotting system into overdrive, increasing clot formation and inflammation, but also suppress natural killer cells — the immune system’s virus-clearing soldiers.”
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
Autopsy study in patients with COVID shows that: SARS-CoV-2 infects, replicates and persists in Macrophages within the coronary vasculature Since CARDIAC MACROPHAGES have a half-life of 8.8years they would act as VIRAL RESERVOIRS in Atherosclerotic plaques
“NEW PREPRINT! Another study about ABNORMAL BLOOD CLOTTING related to SARS-CoV-2, but unlike the others I've covered, this isn't related to the spike protein.
Turns out that Mpro, a viral protease [pro-tee-ace], can START the cascade.
a thread written for everyone:
Here's the takeaway: The Main protease (Mpro) of SARS-CoV-2—an enzyme that cuts up viral polyproteins—can also cleave a few host coagulation factors in a way that ACTIVATES them and BEGINS the blood clot cascade.”
Great analysis thread:
“SIGNIFICANT NEW STUDY PUBLISHED TODAY IN NATURE!
Fibrin ‘binds to the SARS-CoV-2 spike protein,’ forming clots that ‘drive systemic thromboinflammation and neuropathology,’ and it happens ‘independently of active infection.’
Simplified breakdown of the paper below!
