Current postulates support the idea that MS is triggered by an infecti
ous agent or agents through an autoimmune reaction directed against br
ain antigens in genetically susceptible individuals. Evidence for an i
nfectious etiology of MS is indirect. We have proposed that MS may, in
some instances, be due to a zoonotic infection and that canine distem
per virus, a measles-like virus in dogs, is a likely candidate in the
causation of this disorder. The high homology between canine distemper
and measles virus proteins has made it extremely difficult to disting
uish distemper from measles antibodies serologically. We now provide e
vidence that humans can be infected with this neurotropic dog virus. F
urthermore, a high titer of canine distemper virus antibodies is signi
ficantly associated with MS. Identification of the etiologic agent in
MS may lead to the elucidation of disease pathogenesis and to disease
prevention through appropriate public health and vaccination programs.