*4.3.4 Sindbis virus (SV)*

The VS infection in LSU mice is another demyelinating model. This model has not been extensively studied by investigators; however, recent findings indicate that pathogenic infection may cause autoimmune disease [79]. Infected LSU mice develop EAE-like palsy that begins at 6 dpi and lasts up to 8 weeks after infection. Treatment with cyclophosphamide improves the signs of neurological deficits despite the increase in CNS viral load, indicating that paralysis in these mice is mediated by the immune response. CNS lymphocytes taken at 7 dpi are specific to VC, but not to MBP. Interestingly, MBP-specific T cell and Ab responses are found in the peripheral tissues at 8-week post-infection, indicating that anti-myelin responses arise due to bystander damage *via* epitope spreading. The brief common period from SV infection to first neurological deficit indicates that the demyeliationg process is not the primary cause of paralysis, but can contribute to chronic illness [80].
