Several mechanisms have been proposed: activation of the IL-6 and TNFα promoters by B19 NS1 protein during persistent infection,51, 52 molecular mimicry between a B19 VP2 epitope and autoantigens such as collagen II53 and the phospholipase activity of B19 VP1 unique domain with subsequent activation of synoviocytes54 and induction of anti-phospholipid antibodies.55 Recently, B19 NS1 was shown to induce apoptotic bodies containing self-antigens potentially associated with autoimmunity.56 This evidence concerns the gene IL6 and Autoimmunity.