Viral infections frequently elicit strong cellular and humoral immune responses. This bears the inherent danger of co-activating autoreactive lymphocytes, either through bystander activation by cytokines or through direct sharing of conformational determinants between self and virus (mimicry). Autoimmune diseases could then result, even after clearance of the viral infection, if enough autoreactive cells are activated. Alternatively, viral infection of antigen presenting cells can locally enhance inflammation and drive autoreactive lymphocytes. Evidence for these mechanisms, as well as emerging therapeutic concepts, will be discussed.