In spite of the lack of firm evidence implicating infectious agents, it is still likely that SLE requires an initiating event, probably environmental, and possibly infectious. In the setting of genetically determined perturbations of the immune system, an infectious trigger could be a trivial event clinically, and could be different in different patients. Once triggered, the immunologic abnormalities might be self-perpetuating so that the persistent infection and foreign antigens as found in hepatitis B vasculitis, might not be needed in SLE. Current evidence has not firmly implicated any specific microbial agents, but on a theoretical basis, the human retroviruses are particularly attractive candidates.