TY - JOUR
T1 - Recurrent demyelination in chronic central nervous system infection produced by Theiler's murine encephalomyelitis virus
AU - Dal Canto, Mauro C.
AU - Lipton, Howard L.
N1 - Funding Information:
A number of different experimental animal models of demyelination have been described in the literature (Lampert 1978; Paterson 1977). Recently their chronicity has been emphasized because multiple sclerosis (MS), a human demyelinating disease This work was supported in by research grants 1R01 NS-13011 and AI-14139 from the National Institutes of Health.
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1979/8
Y1 - 1979/8
N2 - A morphologic study of demyelination produced by Theiler's encephalomyelitis virus (TMEV) infection in C3H/He mice was performed. Demyelination in this strain of mouse was less intense and had a milder gliomesodermal response than that observed in SJL mice. As early as 80 days after infection numerous remyelinated axons were present in C3H/He mice, and later, extensive remyelination was observed and was mainly by Schwann cells. About one-third of remyelinated plaques showed recurrent demyelinating activity at 200 days. The best evidence of recurrent demyelination was the loss of myelin by axons which had been previously remyelinated by Schwann cells. In addition, acute areas of demyelination were also seen in spinal cords which contained chronic or quiescent plaques. The demonstration of recurrent demyelination in TMEV infection is important for it increases the relevance of this model to multiple sclerosis (MS). In addition TMEV infection of C3H/He mice appears to be an excellent model for further studies of Schwann cell remyelination and recurrent demyelination in the central nervous system (CNS).
AB - A morphologic study of demyelination produced by Theiler's encephalomyelitis virus (TMEV) infection in C3H/He mice was performed. Demyelination in this strain of mouse was less intense and had a milder gliomesodermal response than that observed in SJL mice. As early as 80 days after infection numerous remyelinated axons were present in C3H/He mice, and later, extensive remyelination was observed and was mainly by Schwann cells. About one-third of remyelinated plaques showed recurrent demyelinating activity at 200 days. The best evidence of recurrent demyelination was the loss of myelin by axons which had been previously remyelinated by Schwann cells. In addition, acute areas of demyelination were also seen in spinal cords which contained chronic or quiescent plaques. The demonstration of recurrent demyelination in TMEV infection is important for it increases the relevance of this model to multiple sclerosis (MS). In addition TMEV infection of C3H/He mice appears to be an excellent model for further studies of Schwann cell remyelination and recurrent demyelination in the central nervous system (CNS).
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U2 - 10.1016/0022-510X(79)90172-2
DO - 10.1016/0022-510X(79)90172-2
M3 - Article
C2 - 512673
AN - SCOPUS:0018420758
SN - 0022-510X
VL - 42
SP - 391
EP - 405
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
IS - 3
ER -