Theiler's murine encephalomyelitis virus (TMEV) strains are divided in
to two subgroups on the basis of their differing disease phenotypes. M
embers of the GDVII subgroup, such as GDVII strain, produce an acute l
ethal polioencephalomyelitis. In contrast, members of the TO subgroup,
such as DA strain, induce a persistent infection with chronic demyeli
nation; this white matter disease serves as an experimental model of m
ultiple sclerosis (MS) due to their similar pathology and because the
immune system in both diseases appears to contribute to the demyelinat
ion. The availability of full-length infectious TMEV clones, the relat
ive simplicity of the TMEV genome, and the availability of the mouse a
s a host provide the opportunity to identify molecular determinants an
d disease mechanisms that are responsible for neurovirulence, demyelin
ation and virus persistence, and makes this a valuable system for path
ogenesis studies.