Landmark New Publication: The Forgotten Biochemistry 101 of COVID-19, and Its Critical Consequences
One of the best ways to measure platelet aggregation is the ESR blood test (my favorite single test - but it's never about one thing.) The article below single-mindedly focuses on platelet aggregation. I'm not saying they are right or wrong, but I don't see any lab results to confirm the microscopy conclusions. If you see aggregation like in the image below, ESR will be elevated. But is that the only process going on that can debilitate of kill?
Here are highlights from the paper.
In a paper published April 22, 2024 in Viruses (Basel) [1], an international team of researchers, including two fellows of their nations’ academies of sciences (Colleen Aldous, senior author Wendy Hoy) and others who participated in Nobel prize-honored research (Thomas Borody, Morimasa Yagisawa), has revealed how coronavirus biochemistry well-established over past decades governs the morbidities of COVID-19, risk factors and therapeutic approaches. TrialSite News is pleased to feature this important research.
The glycan monomer sialic acid, ubiquitous on eukaryotic cell surfaces, serves as the initial attachment point to host cells for the COVID-19 virus—SARS-CoV-2—as well as for other coronaviruses. The virus can then slide over to ACE2 for cell entry. SARS-CoV-2 spike protein attaches particularly tightly to the dense sialic acid coatings on the trillions of red blood cells (RBCs), platelets and endothelial cells in the human adult. These interlaced attachments trigger the RBC aggregation, microvascular occlusion and vascular damage underlying the oxygen deficits, blood clotting and related morbidities of severe COVID-19.
In the genetics-centric research environment of recent decades, however, most COVID-19 research ignored this older, well-established biochemistry, focusing instead on SARS-CoV-2 replication and its replication receptor, ACE2. Yet the typical human cell is coated with at most a few hundred ACE2 molecules vs. millions of virally-binding sialic acid molecules. This misdirected focus led to oversights of significant consequence, as detailed in the Viruses paper.
More broadly, disregard for the active physiological role of RBCs yields unreliable or erroneous reporting of pharmacokinetic parameters as routinely obtained for most drugs and other bioactive agents using detection in plasma, with whole blood levels being up to 30-fold higher.
Substantiation of the importance of this glycan biochemistry for COVID-19:
RBC aggregation as experimentally induced in several animal species using an injected polysaccharide, caused most of the same morbidities of severe COVID-19.
Three major risk factors for COVID-19 mortality—older age, diabetes and obesity—are each associated with significantly increased RBC aggregation and microvascular occlusion.
Three generic drugs that gleaned the most interest as COVID-19 therapeutics each reduce blood cell aggregation—one of these, ivermectin, disaggregated virally induced RBC clumps in vitro within 30 minutes.
For mammalian species, clinical susceptibility to COVID-19 correlates to RBC aggregability, with statistical significance (p=0.03).
The two human betacoronaviruses that express a sialic acid-cleaving enzyme, hemagglutinin esterase, are benign, while the other three—SARS, SARS-CoV-2, and MERS—are virulent.
As detailed in the newly published paper and summarized below (see link), this glycan biochemistry is also key to disentangling controversies that have arisen over the efficacy of certain generic COVID-19 treatment agents, one of which, ivermectin, competitively binds to several sites on SARS-CoV-2 spike protein.
Full scientific paper link: https://www.mdpi.com/1999-4915/16/4/647
So is breaking up red blood cell clumps the only consideration? In my case of delta, I also have VERY LOW RBC counts and very high ferritin. This is called anemia of chronic disease (inflammation, infection - multiple terms are used). Breaking up clumping while not solving the low free red blood cell counts will probably NOT restore blood oxygen saturation.
Ivermectin apparently plays a role in breaking up the rouleaux clumps, and we know it has anti-viral properties, so it will help reverse the anemia of chronic disease. But this explains why not everyone recovers - because ivermectin is not a strong antibiotic. Refer to my previous blog where I talk about a multi-treatment approach and why.
The esteemed authors of the full paper do NOT understand anemia of chronic disease. Here is their explanation for the increase in ESR.
Appendix B. Significantly Increased Erythrocyte Sedimentation Rate (ESR), Decreased Hematocrit Level and Increased von Willebrand Factor (vWF) in Severe COVID-19 Patients and Long COVID Patients
Significantly increased blood values for erythrocyte sedimentation rate (ESR) and decreased hematocrit levels were found in severe COVID-19 patients. ESR was increased [50,51,52,53,54], and hematocrit level decreased [55] in COVID-19 patients with greater disease severity, with p < 0.001 for both. This ESR increase is consistent with the RBC clumping induced by SARS-CoV-2 SP (spike protein),
while the decreased hematocrit level could result from larger RBC clumps being sequestered,
NO NO NO - IF THEY MEASURED FERRITIN AND IRON, THEY WOULD HAVE FOUND LOW IRON, CONSISTENT WITH LOW HEMATOCRIT - AND HIGH FERRITIN - THEN THEY WOULD UNDERSTAND THE NEED FOR MULTI-TREATMENTS FOR CO-MORBID VIRALS!
as it occurs for such clumps that form transiently even in healthy mammals, via a distributed network of arterioles and a pulmonary catch–trap architecture [61,62]. Note that RBC aggregation, which is readily reversible, is different from the formation of fibrin-enmeshed blood clots. Also, von Willebrand factor (vWF), an indicator of endothelial inflammation, was sharply increased in severe vs. non-severe COVID-19 patients [195,196] and in COVID-19 [56,57] and long COVID patients [58] vs. controls.
I SEARCHED FOR "FERRITIN" IN THE ARTICLE - AND IT WAS NOT FOUND!
Here is the list of luminaries who do not understand the simple concept of anemia of chronic disease - and how it points BEYOND just the spike protein to CO-MORBID INFECTIONS that the spike/SARS enable to activate/re-activate.
by David E. Scheim 1,,Peter I. Parry 2,3,David J. Rabbolini 4,Colleen Aldous 5,Morimasa Yagisawa 6,7,Robert Clancy 8,Thomas J. Borody 9 andWendy E. Hoy 10
1 US Public Health Service, Commissioned Corps, Inactive Reserve, Blacksburg, VA 24060, USA
2 Children’s Health Research Clinical Unit, Faculty of Medicine, The University of Queensland, South Brisbane, QLD 4101, Australia
3 Department of Psychiatry, Flinders University, Bedford Park, SA 5042, Australia
4 Kolling Institute, Faculty of Medicine and Health, The University of Sydney, St Leonards, NSW 2064, Australia
5 College of Health Sciences, University of KwaZulu-Natal, Durban 4041, South Africa
6 Satoshi Omura Memorial Research Institute, Kitasato University, Tokyo 108-8641, Japan
7 Louis Pasteur Center for Medical Research, Kyoto 606-8225, Japan
8 Emeritus Professor, School of Medicine and Public Health, University of Newcastle, Newcastle, NE1 7RU, Australia
9 Centre for Digestive Diseases, Five Dock, NSW 2046, Australia
10 Emeritus Professor of Medicine, University of Queensland, Herston, QLD 4029, Australia
BTW - ROBERT CLANCY IS OFTEN ON JOHN CAMPBELL'S BROADCASTS. I'VE WRITTEN TO CAMPBELL - BUT APPARENTLY, CLANCY IS SMARTER THAN YOURS TRULY!
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