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Updated: Aug 17, 2026
Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Differential astrocyte response to Theiler's murine encephalomyelitis virus infection
Roberto G Pozner1, Maria I Berría, Soledad Negrotto
1Department of Thrombosis and Haemostasis, Hematological Research Institute, National Academy of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
Objectives:
We aimed to address if selective astrocyte apoptosis is involved in the lack of murine demyelinating disease following infection by the L*-1 variant of Theiler's virus. In addition, we investigated whether L*-1-infected astrocytes were able to selectively express molecules whose effects would play a role as pathogenic factors.
Methods:
Murine cultured astrocytes were infected with two Theiler viruses, the DA strain and the mutated DA variant L*-1, which does not synthesize the out of frame L* protein.
Results:
Neither DA nor L*-1 provoked apoptosis, although they replicated in astrocytes inducing GFAP and iNOS expression, as well as subsequent nitric oxide production. In addition, both viruses caused an enhanced expression of ICAM-1, VCAM-1 and decay accelerating factor (DAF). In this connection, values of VCAM-1 and DAF induced by L*-1 were higher and lower, respectively, than those induced by DA.
Conclusions:
Since no apoptosis was found, such mechanism would not be involved in the lack of TMEV-induced demyelinating disease by L*-1. In contrast, selective expression of VCAM-1 and DAF molecules induced by L*-1 could have a role in virus clearance from the central nervous system.
