In fact, whereas chronically infected mice of a susceptible haplotype (SJL/J mice) showed a severe loss of sodium channel density and intensity along axons, chronically infected β 2 -microglobulin −/− mice showed a dramatic upregulation and redistribution of axonal sodium channels, even though overall levels of myelin loss and distribution of demyelinated lesions were similiar between the two strains (Rivera-Quinones et al., 1998) (Fig. 10) .