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October 1980

Comprehensive Viral Immunology of Multiple Sclerosis: II. Analysis of Serum and CSF Antibodies by Standard Serologic Methods

Author Affiliations

From the Viral and Rickettsial Disease Laboratory, California Department of Health Services (Dr Cremer), Berkeley; the Neurology (Dr Johnson) and Psychiatry (Dr Fein) Services, Veterans Administration Medical Center; the Departments of Neurology (Dr Johnson) and Psychiatry (Dr Fein), University of California, San Francisco; and the Department of Neurology (Dr Likosky), Kaiser Hospital, Santa Clara, Calif.

Arch Neurol. 1980;37(10):610-615. doi:10.1001/archneur.1980.00500590034003

• Sera and CSFs of 85 patients with multiple sclerosis (MS), 49 patients with probable MS, and 165 control patients with other neurologic diseases were assayed for antibodies to rubella, mumps, measles, parainfluenza I (strain 6/94), herpes simplex, cytomegalovirus, varicella-zoster, and vaccinia viruses. Methods included complement fixation (CF), hemagglutination inhibition (HI), and complement-dependent plaque reduction (CPR). Significant differences between the groups with MS and the control groups were higher serum antibody titers to measles virus in the groups with MS, higher proportion of patients with MS with CSF antibodies to measles, rubella, and vaccinia viruses, and greater percentage of patients with MS with more than one CSF viral antibody. Duration and severity of disease in the patients with MS were associated with presence of multiple CSF antibodies. Presence of CSF antibody was positively correlated with the height of the corresponding serum titer, yet a high serum titer did not ensure the presence of CSF antibody. Oligoclonal bands were present in the CSFs of equal proportions of patients with MS with and without CSF viral antibody. Our data support the hypothesis of local antibody synthesis with-in the CNS. However, we favor the view that preprogrammed antibody-forming lymphocytes enter the CNS and then produce antibody either because of nonspecific polyclonal activation in situ or because of failure of normal regulation.

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