COVID-19 coagulopathies: Human blood proteins mimic SARS-CoV-2 virus, vaccine proteins and bacterial co-infections inducing autoimmunity: Combinations of bacteria and SARS-CoV-2 synergize to induce autoantibodies targeting cardiolipin, cardiolipin-binding proteins, platelet factor 4, prothrombin, and coagulation factors.

Abstract

Severe COVID‐19 is often accompanied by coagulopathies such as thrombocytopenia and abnormal clotting. Rarely, such complications follow SARS‐CoV‐2 vaccination. The cause of these coagulopathies is unknown. It is hypothesized that coagulopathies accompanying SARS‐CoV‐2 infections and vaccinations result from bacterial co‐infections that synergize with virus‐induced autoimmunity due to antigenic mimicry of blood proteins by both bacterial and viral antigens. Coagulopathies occur mainly in severe COVID‐19 characterized by bacterial co‐infections with Streptococci, Staphylococci, Klebsiella, Escherichia coli, and Acinetobacter baumannii. These bacteria express unusually large numbers of antigens mimicking human blood antigens, as do both SARS‐CoV‐2 and adenoviruses. Bacteria mimic cardiolipin, prothrombin, albumin, and platelet factor 4 (PF4). SARS‐CoV‐2 mimics complement factors, Rh antigens, platelet phosphodiesterases, Factors IX and X, von Willebrand Factor (VWF), and VWF protease ADAMTS13. Adenoviruses mimic prothrombin and platelet factor 4. Bacterial prophylaxis, avoidance of vaccinating bacterially infected individuals, and antigen deletion for vaccines may reduce coagulopathy risk. Also see the video abstract here: https://youtu.be/zWDOsghrPg8