“…), etc., which revealed that some of the most common autoantigen targets in COVID-19-associated coagulopathies, such as CL, PF4 and β2GP, have significant mimics with these bacteria but do not have significant mimics with SARS-CoV-2 and especially its spike protein [ 40 ] (summarized in Figure 1 ). Since some bacterial infections, especially GAS , Staphylococci, Klebsiella and Clostridia , are themselves associated with increased risks of coagulopathies [ 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 ], these results suggested that preceding or concomitant bacterial co-infections may support the induction of a variety of COVID-19 autoimmune coagulopathies through anamnestic secondary cross-reactivity or bystander activation of complementary autoimmune mechanisms to those activated by SARS-CoV-2. Conversely, if a pre- or co-existing bacterial infection were necessary to induce autoimmune coagulopathies, then the absence of such infections among the vast majority of vaccinees might explain the extremely infrequent occurrence of vaccine-induced thrombotic events [ 62 , 63 ].…”