Abstract
Encephalomyelitis associated with perivenular demyelination occurs as a delayed complication of a wide variety of immunizations and infections. An autoimmune etiology has been postulated both because the pathology and clinical disease closely resemble experimental allergic encephalomyelitis and because infection of the central nervous system has been difficult to demonstrate. Encephalomyelitis following post exposure administration of rabies vaccine prepared from the nervous system of adult animals and occurring late in the course of measles have been most extensively studied in an effort to understand the pathogenesis of this neurological complication. Studies of the immune responses in patients with rabies postvaccinal encephalomyelitis have demonstrated that lymphoproliferative and antibody responses to myelin basic protein (MBP) correlate with development of major neurologic complications and that cerebroside and ganglioside may have an augmentory encephalitogenic role. Studies of postinfectious encephalomyelitis also suggest a pathogenetic role for immune responses to MBP. Investigations of the mechanisms by which such an immune response is induced after diverse viral infections have focused on potential cross-reactivity between viral proteins and MBP and on the role of altered regulation of immune responses during and after infection. There is accumulating evidence that both of these processes may contribute to the development of this demyelinating disease.
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Griffin, D.E., Hemachudha, T., Johnson, R.T. (1989). Postinfectious and Postvaccinal Encephalomyelitis. In: Gilden, D.H., Lipton, H.L. (eds) Clinical and Molecular Aspects of Neurotropic Virus Infection. Developments in Medical Virology, vol 5. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1675-6_18
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