Abstract
The Spike S/Basigin (BSG) interaction, validated in 2020, has since been called putative, postulated, and controversial. Two widely referenced articles have been largely responsible for this. The data presented here demonstrates that the exclusion of this interaction these articles purport to show is due to an inappropriate binding affinity reference value. Spike S/BSG binding avidity is admittedly weaker than that of RH5 (falciparum epitope)/BSG by oligomeric methods, but one cannot then exclude its existence by using a monomeric binding affinity value. Additional clinical and laboratory support for this Spike S/BSG interaction is presented, including the obesity paradox and thrombotic microangiopathy (TMA). Furthermore, BSG is up-regulated in those with comorbidities, something not considered in these two articles.
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