The pathogenesis of acute viral encephalitis and postinfectious encephalomyelitis

Abstract

Japanese encephalitis and postmeasles encephalomyelitis represent two important forms of acute encephalitis in the developing world. Japanese encephalitis accounts for 20,000 acute illnesses per year, and measles encephalomyelitis accounts for as many as 100,000. Both are accompanied by mortalities of 20%-30%, and in both forms, approximately one-half of the survivors have neurological sequelae. Therefore, these two diseases are responsible for a considerable proportion of worldwide mental and motor disabilities. Furthermore, both diseases are preventable with use of safe vaccines. Despite these similarities, their very different pathologies appear to be based on different mechanisms of pathogenesis (table 2). In Japanese encephalitis there is direct invasion of the virus into the nervous system, selective infection and destruction of neurons, and evidence that both humoral and cellular immune responses attenuate the infection. In measles encephalomyelitis there is little evidence that the virus invades the nervous system. Rather, measles virus infects lymphoid cells and causes abnormalities in immune regulation. Humoral immune responses are not found within the nervous system, and the cellular immune response may be inappropriately directed against host antigens. In measles encephalomyelitis, the inflammatory cells entering the nervous system may be the effector cells of autoimmune disease.