These causes included lameness and humane reasons as surrender by owner. None of the horses were ill or demonstrating neurological signs at the time of euthanasia. All horses were necropsied immediately upon euthanasia. Tissues were snap frozen in dry ice and ethanol and stored at 280uC until RNA extraction was performed. Eight tissues were collected from each horse and included cerebrum, cerebellum, thalamus, midbrain, hindbrain, cervical spinal cord, lumbar spinal cord, and spleen. Three analyses were Chloroprocaine hydrochloride established to test the hypothesis that there are gene pathways whose expression changes in a significant and consistent manner due to WNV as a result of exposure status, survival/immune status, and CNS location. With respect to the experimental analyses, three subhypotheses were generated to analyze if there was a difference in gene expression between the nonvaccinated/exposed and untreated horses, the nonvaccinated/exposed and vaccinated/exposed horses, and the nonvaccinated SKI II cerebrum and nonvaccinated thalamus. Blood was drawn from each horse exposed to WNV on post-infection. A PFU assay was performed on the heparinized blood and cells observed for cytopathic effect to determine levels of viremia. Histopathological grading was performed on sections from the thalamus and cerebrum to investigate for the presence of viral encephalitis. Scoring was performed by two blinded and independent pathologists according to previously published data. Lesions were quantified in the pons, medulla, cervical cord and lumbar cord. Briefly cross sections of these areas were examined for the presence of gliosis and perivascular cuffing. One section each was evaluated for the pons and medulla. Two sections were evaluated for each area of the spinal cord. Total numbers of glial nodules were counted in each section. If more than one section was evaluated the counts for these sections were averaged. For pervascular cuffs, 3 areas were examined in each section and 10 vessels were counted in each area. The number of vessels that contained inflammatory cells was divided by the number 10. Each area per section was averaged. Genomic functions analysis links the top transcripts in each pathway to reported disease states and normal function. The functions were distributed amongst many analyses and, in particular, neurological, immunological, and cell death pathways were represented. In horses exposed to WNV compared to normal horses, four categories were identified involving neurological functions, 10 categories were identified involving immunological functions, and 1 category was identified as involving cell death. The genes in the functions from neurological categories were grouped mainly under neurological disease when compared to nervous system development and function, behavior, and psychological disease. When bacteria encounter conditions of low iron, for example during macrophage infection, they produce ironsequestering siderophores in order to maintain cellular functions. Expression of the genes required for mycobactin synthesis is controlled by the regulator of iron homeostasis IdeR. Mycobactin biosynthesis involves the conversion of isochorismate into salicylate by the enzyme MbtI. As a result of this, mycobacteria accumulate salicylate under iron-depleted conditions.