Modern immunology and knowledge of the pathogenesis of systemic lupus erythematosus have expanded enormously over the past decade. No other disease of man better integrates the concepts of autoimmunity, immune-complex disease, lymphocyte heterogeneity and immune regulation; many of these concepts have evolved from studies of the disorder. The evidence for immunologic mediation of the disease is compelling, and yet the etiologic stimulus is unknown: current speculation in this regard is focused on chronic or persistent infection. The observation that endothelial cells of patients with systemic lupus contain tubuloreticular structures resembling paramyxovirus nucleocapsids, as reported in the Journal,1 stimulated studies . . .