PMC:7289100 / 14295-16044 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7289100","sourcedb":"PMC","sourceid":"7289100","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7289100","text":"Therefore, we can assume that aPL can be frequently detected in patients with SARS-CoV-2 infection. Certainly, this finding is not surprising [52]. In fact, the occurrence of transient aPL was described in patients affected by several viral infections such as human immunodeficiency virus (HIV), varicella zoster, hepatitis C virus, cytomegalovirus (CMV), Epstein–Barr virus (EBV), adenovirus, parvovirus B19 [53]. In addition, aPL were also detected in patients with infections of different origin (bacterial, parasitic, etc) and an infection was often reported just before the clinical onset of APS [54]. These observations suggest the possible existence of molecular mimicry due to similarity between the peptide regions identified in the b2GPI molecule (and recognized by anti-b2GPI) and membrane proteins of several virus and bacteria [55]. Animals immunized with different viruses or bacteria (or proteins derived from them) developed anti-b2GPI antibodies that in some cases were associated with the occurrence of thrombosis [56]. The different pathogenic potential of antibodies can be attributed to the fine specificity that they acquire after immunization with different antigens. It is in fact known that antibodies directed to domain 1 of the b2GPI molecule are associated with an increased risk of thrombosis (in systemic autoimmune diseases and APS) [57] while antibodies directed to other parts of the molecule, such as domain 4/5, can be regarded as “innocent” [58]. On the other hand, the features of the host can also be important, since genetic background is recognized as one of the determinant factors in the induction of autoimmunity and can be the driver which turns aPL from being transient to persistent and pathogenic 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