Serum and cells from Theiler's virus-infected mice fail to injure myelinating cultures or to produce in vivo transfer of disease. The pathogenesis of Theiler's virus-induced demyelination appears to differ from that of EAE.

Intracerebral inoculation of SJL mice with Theiler's Murine Encephalomyelitis virus (TMEV) results in a biphasic disease characterized by early grey matter involvement followed by late, chronic white matter inflammation and demyelination. Morphological parameters of TMEV-induced demyelination are essentially identical to those of experimental allergic encephalomyelitis (EAE) and immunosuppression has been shown to prevent demyelination. To test whether the pathogenesis of demyelination in TMEV infection is based on an autoimmune attack on myelin as in EAE, we tested sera and cells from infected animals for their ability to produce in vitro demyelination and cells for their ability to transfer disease in vivo. Isogeneic organotypic cultures were exposed to either serum or splenocytes from diseased animals. Neither serum nor splenocytes demyelinated or prevented myelination in these cultures. Splenocytes from diseased animals were also incubated with basic protein or whole spinal cord and assayed for their proliferative response or their ability to transfer disease to naive recipients. Neither proliferation nor transfer of disease was observed. These results show that the immunopathology of demyelination in the Theiler's model differs from that of EAE in a number of important parameters and support the contention that demyelination in this viral infection is produced by immunological mechanisms different from those operating in EAE.