Abstract
During the last 3 decades a new concept of an infectious process has been derived by studying certain Central Nervous System (CNS) diseases in animals. These infections are characterized by an incubation period lasting for many months to years and by a predictable, protracted clinical course usually leading to death. It has been found that these disorders, which are refered to as slow virus diseases, are related to unconventional and conventional agents, both of which have been associated with naturally occurring diseases in animals and man. The unconventional agents, which have not been visualized, isolated or characterized reveal unusual biological and physico-chemical properties, unlike any known virus group. These agents are associated with scrapie in sheep, encephalopathy in mink and Kuru or Creuzfeldt-Jakob disease in man. The conventional viruses isolated from slow virus diseased brain material, such as Visna, Subacute Sclerosing Panencephalitis (SSPE). Progressive Rubella Panencephalitis (PRP) or Progressive Multifocal Leukoencephalopathy resemble classical viruses with typical structural, physico-chemical and biological characteristics. For this group of viruses, progress has been made in the understanding of the infectious process, since the isolates provide an experimental basis for virological and immunological studies in these diseases. From a pediatric point of view, only SSPE and PRP are of interest, since the other slow virus diseases are usually not seen in children. SSPE is caused by a measles virus infection. Measles virus (refered to SSPE virus) has been isolated from CNS and lymphoid tissue. Moreover the patients reveal a pronounced antimeasles hyperimmunresponse which is pathognomonic for this disorder. Virological studies indicate that SSPE viruses are related but not identical with typical virus isolated from acute measles. At the present state of investigation, SSPE is considered a late complication of acute measles infection. PRP is associated with a persistent rubella virus infection of the CNS. Virological and immunological data reveal great similarities to SSPE, However, information on the pathogenetic mechanism of this disease process are not available. Previous investigations on slow virus diseases have demonstrated the different ways a virus infection can result in a chronic CNS disorder. Moreover, they have shown that virus-host interactions exist which lead to diseases lacking the common characteristics of an infectious process. Obviously, many virological and immunological problems have to be solved before the complexity of these disorders are understood, but it already can be expected, that other human diseases will be found which are caused by a slow virus infection.
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