Autoimmunity with SARS2
November 9th, 2020
"Severe SARS-CoV-2 infection is linked to the presence of autoantibodies against multiple targets, including phospholipids and type-I interferons. We recently identified activation of an autoimmune-prone B cell response pathway as correlate of severe COVID-19, raising the possibility of de novo autoreactive antibody production during the antiviral response. Here, we identify autoreactive antibodies as a common feature of severe COVID- 19, identifying biomarkers of tolerance breaks that may indicate aggressive immunomodulation." (Woodruff et. al. 2020)
A second article in the Journal Science of Translational Medicine found similar issues related to autoantibodies and clotting. Dr. Zou and colleagues found 8 different antiphospholipid antibodies in COVID19 infected patients with clotting issues. These antibodies then recruit white blood cells called neutrophils to the area in question. The end result is a process called neutrophil extracellular traps, NET's, which are highly inflammatory. They found that over half of the admitted patients had these antibodies.
This is a serious problem. The genesis of this issue is caused by the robust host inflammatory response to SARS2. We then sustain aggressive local self tissue and cellular damage. If the cellular debris is repeatedly exposed to the professional antigen presenting cells of the surveillance immune system, then we may undergo the formation of antibodies against these self antigens. The studies above noted that anti-nuclear and antiphospholipid antibodies were found frequently among the ill tested subjects.
They also found many human proteins being targeted for attack including: rheumatoid factor (10/52), prothrombin (2/52), and c-ANCA (2/52). This tells us that the immune system is reacting to disparate tissue types. Woodruff noted that 60% of the patients that had a positive nuclear antibody also had reactivity to another self protein.
These studies coupled with the epidemiological COVID data to date are telling. Humans with dysfunctional metabolics pre COVID illness are at high risk for autoimmune development.
If 77% of deaths are in obese individuals alone and 94+% occur with the big four metabolic chronic diseases, hypertension, coronary vascular disease, diabetes and obesity, then the leap of faith is that the metabolic damage that precedes COVID19 infection from these lifestyle based diseases causes the immune system to overreact to self tissue. We then see the disease play out as cytokine storm and clotting excessively.
Reading the 3 part series on autoimmunity (link below) may help further cement the risks and mitigating circumstances of lifestyle decisions.