Author(s)

Patrick W. Chambers

Department of Pathology, Torrance Memorial Medical Center, Torrance, California, USA.

The primary determinants of Covid severity are ACE genotype, the falciparum antigen (CD147), and vitamin D status. Specifically the I (insertion) and D (deletion) alleles, ACE polymorphisms determine the balance between the RAS (Renin Angiotensin System) and the KKS (Kallikrein Kinin System) in the response to SARS CoV2 (SARS2). CD147, the falciparum antigen, mediates the damage. Vitamin D modulates the immune response. The RAS and KKS connect Covid-19 to Kawasaki’s Disease (KD) and Toxic Shock Syndrome (TSS). Covid-19 pathogenesis is embroiled in a nature versus nurture debate, as it seems to target people of color, unless you live in sub Saharan Africa. There are only three plausible explanations for the latter and they have all been selectively ignored/suppressed by mainstream medicine. This article speaks to the genotypic nature of Covid-19. Angiotensin II, bradykinin, ACE2, ACE and its two polymorphic alleles play vital roles. They predict disease severity. They portend the ARDS variants. They portend extra pulmonary disease or not. The heavily glycosylated CD147 epitope on the spike protein S is key. It has been dismissed as non-existent by flawed studies. Yet its interaction with CD147 receptors on erythrocytes and T lymphocytes cannot be denied and is at the heart of the myocarditis conundrum. Using this key, multiple dots are connected and a red alert issued, whether Covid-19 or vaccine related. These include thrombosis, immune deficit, cancer progression, autoimmune disease, and ADE (Antibody Dependent Enhancement) for those at risk. In susceptible vaccinees its deleterious effects are accelerated. Assessment of this and preventative approaches are explored.

CD147, CD8, Lectin, Glycan, Epitope, Angioedema

Chambers, P.W. (2022) COVID-19: From Cough to Coffin. Open Access Library Journal, 9, 1-24. doi: 10.4236/oalib.1108300.