“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!
"The COVID-19 thrombus has unique and distinct characteristics."
Thrombosis in acute and #LongCovid
“COVID-19, caused by the SARS-CoV-2 virus is an acquired thrombophila with a high incidence of thrombosis.
“Thrombosis…can involve most organs and organ systems.”
Thread by @DickZoutman on Thread Reader App
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus
"The selection of words modulates the message...terms such as “seasonal”, “like a cold”, and “like the flu” can be selected by writers to...lull the reader into a false sense of security... COVID-19 is not primarily a respiratory infection. This virus can cause a systemic disease with far-reaching effects on the body, particularly blood vessels. Once SARS-CoV-2 enters the body, the virus can affect the ...blood vessels, causing inflammation and damage.
It is NOT a pneumonia or pneumonitis It is an immunothrombotic vasculopathy (inflammatory clotting disease)
Latest paper from Dr Robin Kerr & me: #LongCovid is primarily a Spike protein Induced Thrombotic Vasculitis https://researchsquare.com/article/rs-2939263/v1 Here we proposed that long covid is primarily a spike protein-induced thrombotic vasculitis, & we use Robin as a supporting case study 🧵 #TeamClots
Related: "Blood thinners and COVID: The findings guiding patient care"
