Newly described diseases having possible infectious etiology-such as the anti-phospholipid syndrome (APS)-have joined the classical autoimmune conditions. Characterized originally by the triad of manifestations, that is, repeated thromboemboric phenomenon, recurrent pregnancy loss and thrombocytopenia, this disease became eventually one of the most common systemic diseases entailing valve involvement (Liebman-Sacks endocarditis) as well as central nervous system (CNS) affliction (chorea and cognitive impairment). The APS recently was found to be induced by diverse infectious agents. Despite clinical and epidemiologic evidence that many, if not most, autoimmune diseases are triggered by infection, there are very few instances where the underlying mechanisms have been explored. Autoimmune myocarditis in humans often follows infection by enteroviruses. The disease can be reproduced in genetically susceptible strains of mice by infection with a cardiotropic strain of Coxsackievirus B3. This chapter intends to encompass the different mechanisms involved in the infection-autoimmunity association/induction. In addition to molecular mimicry, one will find mechanisms such as polyclonal activation, tissue damage, and the adjuvant effect of the inflammatory process itself.