Severe covid: A postviral autoimmune attack


15-07-21 02:47:00, Autoimmunity to annexin A2 strongly predicts covid mortality (Zuniga et al)

Published: June 15, 2021
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“Severe COVID-19 is NOT a viral pneumonia, but a post-viral autoimmune attack of the lung.”

Note: Patients are asked to consult a doctor.

Already in 2020, multiple studies indicated that severe covid is not just a viral pneumonia, but is in fact a so-called anti-phospholipid antibody syndrome (APS), i.e. an autoimmune attack against phospholipids in endothelial cells that causes hypercoagulation, thrombosis, and respiratory failure.

A new study, published in the European Respiratory Journal, now seems to confirm this hypothesis. Senior author David Lee concludes: “Severe COVID-19 is NOT a viral pneumonia, but a post-viral autoimmune attack of the lung. The target of this autoimmune attack is Annexin A2, a phospholipid-binding protein () ensuring integrity of the pulmonary vasculature and promoting lung elasticity. Antagonism of Annexin A2 would cause lung blood clots, pulmonary edema, and ARDS.”

The chart above shows how anti-Annexin A2 auto-antibodies among hospitalized covid patients strongly predict mortality. Dr. Lee concludes: “It’s time for us to fully reassess how we define the pathophysiology of COVID-19 and consider alternative explanations.” Indeed, the antiphospholipid theory may well explain why most attempts at treating covid patients have failed.

The anti-phospholipid syndrome (APS) is already well-known from other auto-immune diseases, notably rheumatoid arthritis and lupus (SLE). One of the standard medications to prevent APS is, of course, hydroxychloroquine (HCQ). HCQ inhibits APS thrombotic events by inhibiting the anti-phospholipid autoimmune response (the immunomodulatory effect of HCQ) and by inhibiting platelet activation (similar to aspirin). In fact, in patients with autoimmune disease, HCQ and aspirin are often used in combination to achieve optimal results.

In the highly politicized covid debate, both proponents and opponents of HCQ falsely assumed that HCQ would act as an anti-viral drug, which it does not (it also doesn’t act as a zinc ionophore, as a Spanish study showed). As a consequence of this, the design of most HCQ covid studies was misguided (or simply fake,

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