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From Cold to Killer: How SARS-CoV-2 Evolved without Hemagglutinin Esterase to Agglutinate and Then Clot Blood Cells

Scheim, D., Center for Open Science, doi:10.31219/
Oct 2022  
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Ivermectin for COVID-19
4th treatment shown to reduce risk in August 2020
*, now with p < 0.00000000001 from 104 studies, recognized in 23 countries.
No treatment is 100% effective. Protocols combine treatments. * >10% efficacy, ≥3 studies.
4,400+ studies for 79 treatments.
Review of how SARS-CoV-2 evolved to agglutinate and clot blood cells without hemagglutinin esterase (HE). Author proposes a "catch and clump" mechanism where SARS-CoV-2 binds and clumps red blood cells (RBCs) and other cells via sialic acid and CD147, leading to aggregation and occlusion in small capillaries, especially in the lungs. Unlike common cold coronaviruses, SARS-CoV-2 lacks the HE enzyme that could reverse this clumping. The binding occurs through weak individual bonds that cumulatively strengthen with multivalency. Ultramicroscopic studies of COVID-19 tissues show viral spike protein on endothelial cells of capillaries with adjoining alveoli mostly intact, suggesting an initial role of hemagglutination rather than inflammation. Potential factors reducing COVID-19 severity include faster blood flow in the young, blood type O being less agglutination-prone, and common cold coronaviruses reversing RBC clumping via HE. Agents like ivermectin may competitively inhibit SARS-CoV-2 binding to host cells.
Reviews covering ivermectin for COVID-19 include1-41.
Scheim et al., 17 Oct 2022, USA, preprint, 1 author. Contact:
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From Cold to Killer: How SARS-CoV-2 Evolved without Hemagglutinin Esterase to Agglutinate, Then Clot Blood Cells in Pulmonary and Systemic Microvasculature
PhD David E Scheim
The role of vascular occlusion in the morbidities, pulmonary and systemic, of COVID-19 has received increasing focus. Histological studies of lung tissue from COVID-19 patients have found extensively damaged endothelium of capillaries adjoining relatively intact alveoli, corresponding to hypoxemia accompanying normal breathing mechanics in such patients. Essential to the study of vascular occlusion in COVID-19 are viral properties dating back to studies of Jonas Salk in the 1940s that have been positively established for SARS-CoV-2. First, SARS-CoV-2 binds to red blood cells (RBCs) in vitro and also clinically in COVID-19 patients. Second, although fusion and replication of SARS-CoV-2 occur via ACE2, such hemagglutinating viruses initially attach to infective targets and clump with blood cells via much more abundantly distributed glycoconjugate binding sites, notably those tipped with sialic acid (SA). SARS-CoV-2, in particular, attaches to these glycan binding sites. Third, certain enveloped viruses express an enzyme, hemagglutinin esterase (HE), that counteracts viral-RBC clumping. Notably, among betacoronaviruses, the common cold strains express HE while SARS-CoV-2, SARS-CoV-1 and MERS, the virulent strains, do not. The hemagglutinating properties of SARS-COV-2 establish a framework for "catch and clump" induction of microvascular occlusion proposed here. Ultramicroscopic studies of tissues from COVID-19 patients indicate a key role for hemagglutination early and mid-course in COVID-19, before such clumps develop into clots via the coagulation cascade.
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