WNV is thought to replicate at the site of inoculation and then spread to lymph nodes and the bloodstream (6). Viral penetration of the central nervous system appears to follow stimulation of toll-like receptors and increased levels of tumor necrosis factor-α, which increases permeability of the blood-brain barrier (7). WNV directly infects neurons, particularly in deep nuclei and gray matter of the brain, brainstem, and spinal cord (8–10). Collateral destruction of bystander nerve cells may contribute to paralysis (11). Immune-mediated tissue damage may also contribute to pathologic changes in some cases (12). Genetic susceptibility for severe disease in mice has been postulated to involve a deficiency in production of 2´–5´-oligoadenylate synthetase, but this genetic susceptibility has not been elucidated in humans (10). Although most nonfatal WNV infections appear to be cleared by the host immune response, the virus may persist in some vertebrate hosts (10,13).