Abstract
Abstract Antiphospholipid antibodies (aPL) may accompany a response to many infectious agents. The emergence of aPL may be transient or may be associated with the clinical picture of the antiphospholipid syndrome (APS) with manifestations including thrombosis, recurrent fetal loss, central nervous system (CNS), and other organ involvement. The most studied pathogenic aPL are directed to the β 2 glycoprotein I (β 2 GPI) molecule. Studies on experimental APS models have proved that molecular mimicry between β 2 GPI-related synthetic peptides and structures within bacteria, viruses, tetanus toxoid, and cytomegalovirus (CMV) can induce experimental APS. Any explanation of how microbial infections might set off APS must take into account the observation that all individuals appear to harbor potentially autoreactive lymphocytes, as well as natural aPL, but that these cells or antibodies remain innocuous unless somehow activated by a second hit. In this chapter we discuss the associations of aPL in infectious states, molecular mimicry as a proposed cause for the development of APS, aPL vaccination, and drug-induced aPL.
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