As discussed in the preceding chapter, TMEV induces a biphasic disease. The acute phase of disease (first month) is primarily a gray matter disease similar to poliomyelitis. The later chronic disease occurs several months postinfection and is characterized by primary inflammatory demyelination. Immunosuppressive regimens during the acute disease are detrimental because an intact immune system is required to control infection. In contrast, immunosuppression during chronic disease is beneficial because it ameliorates inflammation as the immune response becomes pathogenic (Welsh et al., 1987).
The early immune events that occur during TMEV infection are crucial in the effective clearance of the virus from the CNS. Failure to clear virus results in persistent infection of the CNS and subsequent demyelination (Brahic et al., 1981; Rodriguez et al., 1996). As noted in the preceding chapter 10 (Welsh et al., 2006), innate cytokine responses to infection play an important role in shaping downstream innate and adaptive immune responses (Biron, 1998). For example, the cytokine IFN-ß plays a pivotal role in the early immune response to TMEV (Fiette et al., 1995). Natural killer (NK) cells and CD8+ and CD4+ T cells are also activated early in infection and play an important role in viral clearance (Kaminsky et al., 1987; Welsh et al., 1987; Borrow et al., 1992; Dethlefs et al., 1997; Murray et al., 1998). However, during chronic disease, CD8+ and CD4+ T-cell subsets contribute to demyelination (Clatch et al., 1987; Rodriguez et al., 1988; Welsh et al., 1989).
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