Human multiple sclerosis affects millions of people and is predominately a chronic immune-mediated disease of the central nervous system (CNS). The disease is estimated to affect 2-3 million in 2013 on a global basis. The value of the multiple sclerosis therapeutics market will rise from $17.2 billion in 2014 to approximately $20 billion by 2024. However, the pathogenic mechanisms underlying disease progression are not understood and currently there is no cure for the disease. Therapeutic drugs are developed using two classical experimental autoimmune/allergic encephalomyelitis (EAE) models. Experimental autoimmune/allergic encephalomyelitis (EAE) is the most extensively studied animal model for human MS. However, EAE mainly affects spinal cord white matter, whereas human MS displays demyelination and axonal injuries in the cerebral and cerebellar cortex. In addition, human MS progression cannot be studied in EAE.The second major animal model is RNA virus (TMEV, Theiler’s murine encephalomyelitis virus) induced demyelination, which is considered as a more relevant model to human MS. However, demyelination is caused by persistent TMEV virus infection that is not observed in human MS. Additionally, the TMEV virus can only infect mouse, but not other rodents or primates, limiting its utilization in establishing MS models in other species. Because the TMEV virus is a mouse pathogen, animal facilities often refuse such studies. A new animal model that more closely resembles the pathology of human multiple sclerosis is urgently needed.