INS and infection: Infection with a virus, such as CV-B4, can result in the activation of an endogenous factor, in this case HERV-W ENV, whose pathogenic effects have been reported: inhibition of insulin secretion by β cells, induction of autoimmunity by molecular mimicry, and superantigen-like activity exacerbating the immune response against pancreatic cells [3,44,45,46].