Experimental allergic encephalomyelitis: Modification of optic nerve pathology by antecedent virus infection

Strain 13 guinea pigs, sensitised with spinal cord and Freund's complete adjuvant at 18–21 days of age, developed an experimental allergic encephalomyelitis (EAE) characterised by a non-fatal first attack followed by recovery, then remissions and relapses in the majority of animals. Pretreatment with an i.p. injection of an avirulent strain (A 774) of Semliki forest virus at 1 day of age resulted in an EAE with an accelerated onset and enhanced mortality during the first attack. Unlike the acute phase pathology in unpretreated animals, optic nerve demyelination was observed at 14 days after neuroantigen sensitisation. In sections of optic nerve from virus-treated animals, endothelial cell vesicularisation was seen and the role of this change in disease exacerbation is discussed. Virus treatments of animals older than 1 day of age resulted in a failure to potentiate the disease. Virus inoculated simultaneously with spinal cord alone failed to act as an adjuvent. The mechanism of virus action in modifying the immunopathogenesis of EAE and its relevance to multiple sclerosis is discussed.