Perforin-deficient mice did not acquire hind-limb paralysis, did not show a decrease in spontaneous activity, and did not develop signficant changes in hind-limb stride, suggesting that neurological deficits associated with demyelination are dependent on perforin, and, by extension, on functional cytotoxic T-cells (Murray et al., 1998) . Furthermore, we have recently observed that the number of large axons in the spinal cord does not differ between infected wild-type C57BL/6 mice and perforin-deficient C57BL/6 mice, strengthening the argument that neurological function in these animals is preserved as a result of axon preservation.