We studied 19 patients with postinfectious encephalomyelitis complicating natural measles-virus infections, and our results support the hypothesis that this demyelinating disease has a pathogenesis similar to that of experimental allergic encephalomyelitis. Early myelin destruction was demonstrated by the presence of myelin basic protein in cerebrospinal fluid, and lymphocyte proliferative responses to myelin basic protein were found in 8 of 17 patients tested. A lack of intrathecal synthesis of antibody against measles virus suggests that measles encephalomyelitis may not be dependent on virus replication within the central nervous system. Similar lymphoproliferative responses to myelin basic protein of lymphocytes from single patients with encephalomyelitis after rabies vaccine or after varicella or rubella virus infections suggest a common immune-mediated pathogenesis for the perivenular demyelinating disease that can follow the injection of neural tissues or infection by a variety of viruses. (N Engl J Med 1984; 310:137–41.)

Measles is associated with alterations in immune regulation that sometimes lead to secondary infections or autoimmune encephalomyelitis. Simultaneously, an effective measles virus–specific immune response develops. To relate immune activation to measles and its complications, we studied the spontaneous proliferation of blood mononuclear cells and circulating levels of soluble interleukin-2 receptor and CD8 T-cell antigens in 126 patients with complicated or uncomplicated measles at various stages of the disease.

Using peroxidase immunohistochemistry and in situ hybridization to localize viral antigen and RNA, we studied autopsy tissues from 20 cases of acute fatal human measles (including seven patients with acute encephalomyelitis) and peripheral blood mononuclear cells from 16 patients with acute, nonfatal measles. In immunologically normal patients, virus was detected in five of nine who died five days or less after the onset of rash but in noneof 11 who died later. Virus was localized to epithelial cells of lung, gut, bile duct, bladder, and skin and to lymphoid organs. Neither viral antigen nor RNA was detected in brain sections from 14 patients, including seven with acute encephalomyelitis and four with virus identified in other tissues, a finding supporting an indirect pathogenesis of post-measles encephalomyelitis. These data show that measles virus replicates in cells previously not recognized to be involved (capillary endothelium of lymph nodeand thymus, Hassall's corpuscles, and hepatic duct epithelium) and that invasion of the brain parenchyma during acute measles is uncommon.