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Although the pathogenesis of multiple sclerosis remains obscure, much pathological and clinical evidence suggests an infective agent as a possible aetiological factor. If such an agent is responsible for initiating the disease it seems probable that there is a latent period of several years before the develop ment of clinical features of multiple sclerosis. By that time it might be impossible to obtain laboratory evidence of the incriminating organism. However, if the agent remained latent in the central nervous system it might provide a constant anti genic stimulus manifesting itself in high antibody levels. In a previous study (Ross, 1962) sera from 40 cases of multiple sclerosis were examined by complement-fixation (C.F.) technique for antibodies to several viral and rickettsial antigens. Mainly negative findings were obtained for lymphocytic chorio meningitis, louping-ill, Q fever, murine typhus, and rickettsial pox. Antibodies were detected for herpes in 33 (82%), for mumps in 29 (72%), and for the psittacosis-lymphogranuloma group (P-LGV) in 4 (10%). However, the absence of controls in this investigation meant that no significance could be placed on the positive findings. Thus a further investigation was required to compare antibody levels in a series of cases of multiple sclerosis with those obtained in a series of carefully matched controls.
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Ross et al. (1965) studied this question.
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